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2-pharm Exam > SSRI's/Tricyclic's > Flashcards

SSRI's/Tricyclic's Flashcards

1
Q

what is the most broad class of antidepressants used as first line for panic disorder and obsessive compulsive syndrome

A

SSRI’s

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2
Q

SSRI’s are also effective for what two additional issues

A

social phobia and post traumatic stress disorder

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3
Q

what pathways do newer SSRI acton in the brain

A

serotonin and norepinephrine

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4
Q

why is it possible to switch a person from one SSRI to a different SSRI if they dont do well on the first one

A

SSRI hav different side effect profiles- making it good to swap to a different SSRI if one doesn’t work. must try several different ones before moving on to a different one

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5
Q

what receptors are involved in the etiology of anxiety

A

serotonin

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6
Q

what is necessary for the effective treatment of obsessive compulsive disorder

A

potent inhibition of serotonin reuptake.

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7
Q

when comparing tricyclic antidepressants to SSRI- what is the most important advantage of SSRI compared to tricyclic

A

relative safety when taken in overdose.

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8
Q

name the one SSRI that is dangerous if taken in overdose

A

venlafaxine- proconvulsant and cardiac side effects

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9
Q

name the 4 comparisons of SSRI to tricyclic antidepressants

A

lack anticholinergic properties
do not cause postural hypotension
no delayed conduction of cardiac impulses
do not appear to have a major side effect on the seizure threshold

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10
Q

what is the prominent cause of SSRI noncompliance

A

sexual dysfunction

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11
Q

what are the 5 common side effects of SSRI

A 
insomnia
agitation
headache
nausea 
diarrhea
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12
Q

Abrupt d/c with short acting half times (paroxetine, venlafaxine) may be associated with

A 
Dizziness
Paresthesias
Myalgias
Irritability
Visual disturbances
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13
Q

SSRI with short elimination half times how do we discontinue them

A

taper them

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14
Q

what is the black box warning for SSRI

A

suicidal tendencies in children and adolescents

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15
Q

for management of anesthesia with SSRI-what do these patients have increased risk of? How do we manage that

A

bleeding as SSRI have an anti platelet activity

may consider holding anti platelet medication in the perioperaive setting if their

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16
Q

what is the washout time for SSRI and reinitiating may require how many weeks for reestablishment

A

washout 2-3 weeks

reinitiating 2-4 weeks

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17
Q

if we discontinue SSRI what are we risking? who should discontinue them

A

major depressive episode- have the ordering provider discontinue them

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18
Q

how does trazodone work

A

inhibits serotonin reuptake and may act as a serotonin agonist via active metabolite

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19
Q

what is trazodone used best as

A

treatment of insomnia

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20
Q

venlafaxine MOA

A

inhibits the reuptake of norepinephrine and serotonin and may potentiate the action of dopamine in the CNS

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21
Q

what is venlafaxine effect on BP

A

increase in diastolic blood pressure

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22
Q

T?F venlafaxine can be beneficial for neuropathic pain

A

true

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23
Q

bupropion MOA

A

inhibit dopamine and Norepinephrine uptake

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24
Q

bupropion uses

A

major depression

smoking cessation

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25
Q

bupropion is associated with what incidence greater than other antidepressants

A

greater incidence of seizures

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26
Q

is bupropion associated with sexual dysfunction

A

no

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27
Q

sertraline causes more ___compared to fluoxetine

A

nausea, diarrhea

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28
Q

when is fluoxetine administered

A

once daily in the am. every other day due to prolonged elimination half time.

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29
Q

how many weeks does fluoxetine need for washout prior to maoi medication

A

5 weeks

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30
Q

what is the first most inhibitor of p-450 and the second most inhibitor of p-450

A

fluoxetine is the most potent inhibitor followed by a less potent inhibitor sertraline

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31
Q

MAOI plus fluoxetine result in what development

A

serotonin syndrome

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32
Q

fluoxetine and lithium or carbamazepine may also develop

A

serotonin syndrome

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33
Q

what drug was most commonly used prior to SSRI

A

tricyclic antidepressants

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34
Q

what are the three side effect profiles seen with tricyclic

A

anticholinergic properties
antiadrenergic properties
antihistamine properties

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35
Q

what is the therapeutic index of tricyclic and what level do you see toxicity

A

100-300

greater than 500

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36
Q

it is preferable to taper tricyclic and tetracyclic antidepressants during a 4 week period to avoid

A

chills
coryza
muscles aches

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37
Q

in low doses what can amitriptyline and imipramine be used to treat

A

chronic neuropathic pain and other chronic pain syndromes-fibromyalgia

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38
Q

tricyclic antidepressants produce anti-inflammatory effects similar to what drug

A

local anesthetics

39
Q

why is efficacy limited for tricyclic treatment of chronic pain syndromes

A

narrow therapeutic index range + intolerability of side effects

40
Q

prototype of tricyclic antidepressants

A

Imipramine

41
Q

what two things does the structure of tricyclic antidepressants resemble

A

local anesthetics and phenothiazine

42
Q

which tricyclic enhances central norepinephrine and serotonin activity in the CNS

A

mirtazapine

43
Q

the clinical profile of maprotiline resembles

A

imipramine

44
Q

maprotiline and mirtazaine should not be given with

A

MAOI

45
Q

secondary amines are primarily what type of reuptake inhibitors

A

NE

46
Q

teriteray amines are primary what type of uptake inhibitors

A

NE and serotonin

47
Q

tricyclic antidepressants work how soon

A

2-3 weeks

48
Q

chronic administration of tricyclic antidepressants decrease sensitivity to which receptors

A

postsynaptic B1
Serotonin2
presynaptic a2

49
Q

chronic administration of tricyclic antidepressants INCREASES sensitivity to which receptors

A

alpha 1

50
Q

metabolism of imipramine

A

metabolized to its active compound desipramine. Both are inactivated by oxidation of hydroxyl metabolites and by conjugation with glucuronic acid.

51
Q

Nortriptyline metabolism

A

Nortriptyline is the active demethylated metabolite of imipramine and amitriptyline and can accumulate to levels that exceed the precursors

52
Q

Doxepin metabolism

A

appears to be converted to active metabolite nordoxepin by demethylation

53
Q

which tricyclic has the highest incidence of anticholinergic effects (dry mouth, blurred vision, tachycardia, urinary retention, slowed gastric emptying, ileus)

A

amitriptyline

54
Q

which tricyclic has the fewest effects with anticholinergic effects

A

desipramine

55
Q

at which tricyclic doses do you see anticholinergic effects

A

high doses

56
Q

which population has the highest incidence of anticholinergic effect even at therapeutic doses

A

elderly

57
Q

what two reasons do the elderly have the highest incidence of anticholinergic effects even at therapeutic doses

A
  1. greater sensitivity to anticholinergic effects compared to young people
  2. reflects polypharmacy (OTC for diarrhea or insomnia)
58
Q

what is the most common cardiovascular side effect of tricyclic antidepressants

A

orthostatic hypotension

modest increases in heart rate

59
Q

what population does tricyclic orthostatic hypotension affect the most

A

elderly patients - increased risk of fractures when they fall.

60
Q

what is the risk of hypotension during general anesthesia in patients taking tricyclic

A

low risk- but has been reported

61
Q

in the absence of severe preexisting cardiac dysfunction, what properties exist for tricyclic antidepressants

A

cardiac antidysrhythmic properties

62
Q

what EKG changes does tricyclic antidepressants possess.

Are these EKG changes worrisome

A

prolong PR interval
widening QRS
Flattening or inversion of the T wave
benign changes- disappear with continued therapy

63
Q

what medication is used when someone on tricyclics has dangerously slow atrioventricular or intraventricular conduction of cardiac impulses

A

Atropine!!

64
Q

the Direct cardiac depressant effect of tricyclics reflect which drug actions on the heart

A

quinidine- due to the slowing of sodium ion flux into cells resulting in altered depolarization and conduction of cardiac impulses

65
Q

what CNS effect seen with tricyclic may be desirable for management of depressed patients with insomnia

A

sedation

66
Q

what two tricyclic produce the greater degree of sedation

A

amitriptyline and doxepin

67
Q

what is the concern with maprotiline and clomipramine administration

A

lower the seizure threshold =is it safe to administer these drugs to patients with seizure disorders

68
Q

what population is most sensitive to seizure inducing effects of tricyclic antidepressants

A

children

69
Q

which anesthetic gas are we concerned about CNS stimulating effects when combined with tricyclic

A

enflurane

70
Q

weakness and fatigue are seen in patients treated with tricyclic’s similar to what medication

A

phenothiazines- like who cares?!?

71
Q

do extrapyramidal reactions occur with tricyclic

A

no

72
Q

what percent of patients -especially the elderly -develop a fine tremor

A

10%

73
Q

tricyclic overdose can be fatal due to what three occurances

A

cardiac toxicity
tendency to cause seizures
CNS depressants

74
Q

combination of tricyclic and MAOI result in CNS toxicity resulting in what three things

A

hyperthermia
seizures
coma

75
Q

tricyclic binding to plasma albumin can be decreased by competition from:

A

Phenytoin
Asa
Scopolamine

76
Q

what type of acting sympathomimetic may produce exaggerated pressor response due to increased amount of norepinephrine available to stimulate postsynaptic adrenergic receptors

A

Indirect acting and direct acting

77
Q

for patients taking chronic tricyclic (>6weeks) administration of either direct or indirectly sympathomimetic - how much do we change the dose

A

one-third the usual dose

78
Q

in patients - a potent direct-acting sympathomimetic should be administered such as

A

NE

79
Q

is the dose of exogenous EPI increased or decreased during anesthesia needed to produce cardiac dysrhythmias

A

decreased!

80
Q

in theory - what medication would be best to give to a patient on tricyclics to avoid anticholinergic

A

glycopyrrolate

81
Q

are tricyclics synergistic with opioids

A

yes

82
Q

what tolerances develop with tricyclic

A

tolerance to anticholinergic effects

tolerance does not develop to antidepressant effects.

83
Q

overdose of tricyclic antidepressants is considered

A

life threatening

can quickly become unresponsive

84
Q

what are the most frequent terminal events.

A

Intractable myocardial depression or ventricular cardiac dysrhythmias are the most frequent terminal events.

85
Q

physostigmine dose for anticholinergic effects

A

0.5-2mg IV

86
Q

what is seen on the EKG- with tricyclic antidepressants

A

prolonged QRS

87
Q

comatose phase last in tricyclic antidepressants

A

24-72

88
Q

during overdose what do you give for seizures

A

benzo

89
Q

what is the quickest thing we can give to help alkalization of the plasma (PH>7.45)

A

hyperventilation.

90
Q

whats the second thing you can do to alkalization with tricyclic overdose

A

sodium bicarb

91
Q

what two drugs help suppress cardiac ventricular dysrhythmias

A

phenytoin

lidocaine

92
Q

does HD or diuresis work to remove overdose of tricyclic antidepressants

A

no

93
Q

gastric lavage / activated charcoal may be helpful but what must you do

A

have a cuffed tube to avoid aspiration

2-pharm Exam (10 decks)

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