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pharm test #5 > Antidepressants > Flashcards

Antidepressants Flashcards

1
Q

to make serotonin, what is needed?

A

tryptophan

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2
Q

what are the side effects of SSRIs?

A

tremors (intentional tremor), nausea, headache, agitation, nervousness, loss of labito and sexual function

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3
Q

why does it take several weeks for SSRIs to be effective?

A

-they increase the serotonin in the synaptic cleft, but with that increase, the serotonin (5-HT) acts on the auto receptors which in turn down regulate the production of serotonin. Eventually, the SSRIs produce desensitization of the auto receptors, and it takes a while for this to happen

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4
Q

serontonergic syndrome

A

bc of the increase of serotonin from SSRIs and SNRIs patients can have

  • tachycardia, htn,
  • psychiatric manifestations (manic, elevated mood, confusion, hyperactivity),
  • GI (cramping, bloating, diarrhea), and
  • neurological (tremolo usness, incoordination)
  • Big ones: diaphoresis (sweating), hyperthermia, and death by cardiovascular collapse
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5
Q

drug interactions of SSRIs and SNRIs

A

with MAO inhibitors the admin of antidepressants within 2 weeks of the discontinuation of MAO inhibitors can rest in SEVERE HYPERTENSIVE CRISIS or in the case of SSRI’s a serotonin syndrome consisting of hyperthermia, muscle rigidity and confusion

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6
Q

which antidepressant produces severe discontinuation syndrome if not tapered off?

A

Paxil

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7
Q

how would you treat an overdose of antidepressants? (esp tricyclics)

A

Physostigmine

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8
Q

what drug(s) is/are used to treat serontonergic syndrome?

A

cyproheptadine (oral) and chlorpromazine (IV)

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9
Q

Fenfluramine

A

a 5-HT (serotonin) releasing drug

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10
Q

fluoxetine

A

blocks reuptake of 5-HT (serotonin) and thus increases 5-HT

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11
Q

what does MAO do?

A

degrades 5-HT (serotonin) to HIAA

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12
Q

which drugs (class) block the reuptake of monoamines (particularly NE and/or serotonin) into presynaptic neurons

A

tricyclic antidepressants and SSRI’s

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13
Q

what are the original tricyclic antidepressants?

A
  • imipramine and its N-demethylated counterpart DESIPRAMINE. also
  • amitriptyline and it’s N-demethylated counterpart NORTIPTYLINE and
  • Doxepine
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14
Q

how do tricyclic antidepressants work?

A

-block the reuptake of NE and Serotonin

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15
Q

which tricyclics have a greater specificity for serotonin and what are they more useful for?

A

the tertiary amines (imipramine and amitriptyline) and are somewhat more sedating

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16
Q

which tricyclics have greater specificity for NE?

A

the demethylated secondary amines (desipramine and nortriptyline), these are less sedating

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17
Q

this drug is relatively specific for dopamine uptake inhibition, lacks sedative effects, has a low incidence of anticholinergic effects, but may be associated with an increased risk of seizures

A

Buproprion (Wellbutrin)

-it is a “second generation” antidepressant

18
Q

the drug is approved specifically for txt of obsessive -compulsive disorders (OCD). In most respects its pharmacology resembles nonselective tricyclics

A

Clomipramine (Anafranil)

19
Q

which drug is the most commonly used antidepressant?

A

Fluoxetine (Prozac)

20
Q

compare the side effects of SSRI’s and traditional tricyclics

A
  1. They are less likely to cause sedation, orthostatic hypotension, ! !tachycardia, cardiotoxicity, seizures, weight gain, blurred vision or dry !mouth. !
  2. The most frequent side effects of SSRI’s are nausea, headache, tremor, !insomnia or somnolence, agitation and nervousness. !
  3. They are at least as likely as tricyclics to cause impairment of sexual !function, presenting a significant problem for many patients. !
  4. There is also some question whether they are as effective as older tricyclics !for severe depression and would not be as useful for depressed patients who !would benefit from some sedation. Fluoxetine and fluvoxamine have been !specifically approved for treatment of OCD
21
Q

what drugs could be used to treat OCD?

A
  • clomipramine
  • fluoxetine (prozac)
  • fluvoxamine
22
Q

which drug has dual action and thus blocks the reuptake of both 5-HT and NE?

A

venlafaxine

-mirtazepine also has dual action, it has serotonergic and noradrenergic effects

23
Q

which antidepressant has a long duration of action and active metabolites that can lead to accumulation and slow return to drug-free status. (thus a shorter duration drug may be indicated is some cases like elderly pts)

A

-fluoxetine (prozac)

24
Q

***chronic txt of animals with SSRI antidepressants causes:

A
  • desensitization and down-regulation of serotoninergic auto receptors that regulate:
  • the firing rate of raphe neurons (somatodendritic auto receptors)
  • the synthesis of serotonin (presynaptic auto receptors)
  • the release of serotonin (presynaptic auto receptors)
  • A marked increase in synaptic levels of 5-HT in the continued presence of uptake blockade as a result of removal of the negative feedback loops by desensitization and down-regulation
25
Q

which SSRI’s are long acting?

A

Fluoxetine and paroxetine

26
Q

which drugs inhibit cytochrome P450 enzymes? and thus increase bleeding in what situation?

A

Fluoxetine and paroxetine

-they may increase the incidence of bleeding with WARFARIN and decrease the bioavailability of phenytoin and digoxin

27
Q

the ____ properties of the tricyclics are additive with atropine and related drugs

A

anticholinergic

28
Q

antidepressants with seizure potential should be used cautiously in combination with…

A

drugs that lower seizure thresholds (e.g. phenothiazines)

29
Q

discontinuation syndrome

A

rapid discontinuation of medication can result in insomnia, nausea, headaches and flu-like symptoms, pts should taper off for 2-4 weeks

30
Q

what is the effective antidote for antidepressant overdose?

A

Physostigmine

31
Q

which are more toxic in overdose cases: SSRI’s or the older tricyclics?

A

older tricyclics are more toxic

32
Q

antidepressants have what effect on sleep?

A

they suppress REM sleep and increase slow-wave sleep

-ppl with short REM are more likely to develop depression

33
Q

what are the monoamine transmitters?

A
  • catecholamines: dopamine, NE, and epi

- Indolamines: serotonin (5-HT)

34
Q

what is the principle MAO inhibitor in use?

A

tranylcypromine (parnate)

others include: phenelzine and isocarboxazide

35
Q

which MAO inhibitor is marketed as an antihypertensive agent although there is little pharmacological basis for differentiating it from other MAO inhibitors?

A

pargyline

i don’t know if we need to know it

36
Q

what are the two types of MAO and where are they found?

A
  • MAO-A (found in NE and serotonin nerve terminal)

- MAO-B (found in Dopamine secreting neurons)

37
Q

inhibition of MAO-A is responsible for …

A

antidepressant activity

38
Q

inhibition of MAO-B is responsible for …

A

the side effects of MAOIs, most MAOIs act on both MAO-A and B

39
Q

medication prescribed as treatment for mood disorders can result in… (side effects, specific to dental)

A
  • dry mouth
  • increased caries
  • pd disease
40
Q

when taking MAOIs, what should not be ingested?

A
  • tyramine, found in cheeses, red wine, avocados, beer. These are normally metabolized by MAO
  • sympathomimetic amines (present in many OTC cold remedies and diet pills) and Levodopa and tricyclic antidepressants taken before MAOI clears
  • these can produce HYPERTENSIVE CRISIS
41
Q

severe serotonin toxicity symptoms

A

-rapidly rising temperature
-respiratory failure (hypertonia/rigidity)
-spontaneous clonus (involuntary muscle contractions)
(htn, tremors, tachycardia, mydriasis (dilated pupils))

pharm test #5 (2 decks)

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