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Psych: Test 1 > Pharm: Antidepressants > Flashcards

Pharm: Antidepressants Flashcards

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1
Q

Citalopram

A
  • SSRI -

MOA: selective seratonin reuptake inhibitor: inhibit seratonin transporter (SERT), thus increasing concentration of seratonin in cleft

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2
Q

Escitalopram

A
  • SSRI

MOA: selective seratonin reuptake inhibitor: inhibit seratonin transporter (SERT), thus increasing concentration of seratonin in cleft

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3
Q

Sertraline

A
  • SSRI

MOA: selective seratonin reuptake inhibitor: inhibit seratonin transporter (SERT), thus increasing concentration of seratonin in cleft

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4
Q

Selegiline

A

MAOI

MOA: monoamine oxidase inhibitors prevnt metabolism of NE and 5-HT and DA:
= selective irreversible MAO-B inhibitor at low doses (useful in Parkinson’s disease) and nonselective MAO-A/B inhibitor at higher doses (used to treat refractory depression)

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5
Q

monoamine hypothesis

A

i) Depression is caused by a decrease in biogenic amines (primarily NE and 5-HT, but also DA); excess biogenic amines results in mania and psychotic states
ii) All currently available antidepressant drugs are classified as having as their primary mechanism of actions on the metabolism, reuptake, or selective receptor antagonism of serotonin, norepinephrine, or both
iii) Depletion of biogenic amines with reserpine, which blocks vesicular uptake of monoamines and depletes their concentration in nerve endings, can induce depression in normal individuals
iv) LSD is a 5-HT2A receptor agonist that causes hallucinations and altered mental states
v) Anti-adrenergic drugs can induce depression

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6
Q

receptor hypothesis

A

i) Some antidepressants decrease NE and/or 5-HT receptor density in particular brain regions or decrease the sensitivity of these receptors to stimulation
ii) Antidepressants may take 1-4 weeks to produce any improvement and 6-8 weeks to achieve substantial benefit; The acute pharmacological effects of these drugs on neurotransmitter levels and subsequent receptor activation are immediate (minutes)
iii) This lag in onset of clinical efficacy implies that dynamic changes in neural circuits must occur before benefits can be realized; This probably involves regulation of receptor signaling, cellular sensitivity to signals, and trophic factor-induced changes in neuronal plasticity

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7
Q

Fluoxetine

A
  • SSRI

MOA: selective seratonin reuptake inhibitor: inhibit seratonin transporter (SERT), thus increasing concentration of seratonin in cleft

USE: depression, eating disorders, OCD

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8
Q

Fluvoxamine

A
  • SSRI (labeled for OCD)

MOA: selective seratonin reuptake inhibitor: inhibit seratonin transporter (SERT), thus increasing concentration of seratonin in cleft

USE: depression, OCD

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9
Q

Paroxetine

A
  • SSRI

MOA: selective seratonin reuptake inhibitor: inhibit seratonin transporter (SERT), thus increasing concentration of seratonin in cleft

USE: depression, OCD

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10
Q

receptor hypothesis

A

i) Some antidepressants decrease NE and/or 5-HT receptor density in particular brain regions or decrease the sensitivity of these receptors to stimulation
ii) Antidepressants may take 1-4 weeks to produce any improvement and 6-8 weeks to achieve substantial benefit; The acute pharmacological effects of these drugs on neurotransmitter levels and subsequent receptor activation are immediate (minutes)
iii) This lag in onset of clinical efficacy implies that dynamic changes in neural circuits must occur before benefits can be realized; This probably involves regulation of receptor signaling, cellular sensitivity to signals, and trophic factor-induced changes in neuronal plasticity

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11
Q

first line MMD and anxiety?

A

SSRIs- fewer antimuscarinic side effects and are less cardiotoxic in overdose

SNRI’s, bupropion and Mirtazapine as well

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12
Q

tx for patient who can’t tolerate sexual dysfunction, weight gain, and sedation that may occur with other antidepressants?

A

bupropion - but generally is not effective for treatment of anxiety

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13
Q

second and third choice for MMD tx?

A

x) TCAs and MAOIs are relegated to second- or third-line treatments for MDD; they are potentially lethal in overdose, require titration to achieve therapeutic dose, have serious drug interactions, and have many adverse effects; However, these drugs remain valuable alternatives for patients with moderate to severe depression who do not respond to an SSRI or SNRI

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14
Q

suicidality?

A

all antidepressants increase risk of suicidal ideation and gestures - however decrease the risk of completed suicides

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15
Q

SNRI’s AEs?

A

** have the serotonergic side effects exhibited by SSRIs but also have noradrenergic SE’s: insomnia, anxiety, and agitation

** Elevated blood pressure and heart rate are sometimes an issue

  • Discontinuation syndrome like that seen with SSRIs
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16
Q

TCA AE’s?

A
  • Anticholinergic effects : drowsiness, dry mouth, constipation, urinary retention, blurred vision, and confusion
  • Orthostatic hypotension due to α-adrenergic receptor blockade, especially in the elderly
  • Weight gain and sedation due to H1 histamine receptor antagonism
  • Cardiotoxicity, arrhythmias and heart block; Convulsions; hepatic dysfunction; Hyponatremia, which may lead to confusion in the elderly
  • Hematological abnormalities (e.g., leucopenia, thrombocytopenia and agranulocytosis)
  • Sexual side effects similar to those seen with SSRIs
  • Discontinuation syndrome like that seen with SSRIs

Contraindications: Arrhythmias, recent myocardial infarction, liver disease, glaucoma, mania

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17
Q

Selegiline

A

MAOI

MOA: monoamine oxidase inhibitors prevnt metabolism of NE and 5-HT and DA:
= selective irreversible MAO-B inhibitor at low doses (useful in Parkinson’s disease) and nonselective MAO-A/B inhibitor at higher doses (used to treat refractory depression)

AE’s:

  • Orthostatic hypotension and weight gain
  • Highest rates of sexual side effects of all the antidepressants; anorgasmia is common
  • May cause dangerous interactions with certain tyramine-containing foods and with serotonergic drugs (see “Drug Interactions” below)
  • Sudden discontinuation syndrome manifested in delirium-like presentation with psychosis, excitement, and confusion
18
Q

TCA AE’s?

A
  • Anticholinergic effects : drowsiness, dry mouth, constipation, urinary retention, blurred vision, and confusion
  • Orthostatic hypotension due to α-adrenergic receptor blockade, especially in the elderly
  • Weight gain and sedation due to H1 histamine receptor antagonism
  • Cardiotoxicity, arrhythmias and heart block; Convulsions; hepatic dysfunction; Hyponatremia, which may lead to confusion in the elderly
  • Hematological abnormalities (e.g., leucopenia, thrombocytopenia and agranulocytosis)
  • Sexual side effects similar to those seen with SSRIs
  • Discontinuation syndrome like that seen with SSRIs

Contraindications: Arrhythmias, recent myocardial infarction, liver disease, glaucoma, mania

19
Q

which antidepressants seen more often in OD?

A
  • TCAs are the most toxic of all the antidepressants, particularly amitriptyline, especially when taken in overdose, which can lead to arrhythmias, altered mental status, and seizures
  • MAOIs are also potentially lethal in overdose producing autonomic instability, hyperadrenergic symptoms, psychotic symptoms, confusion, delirium, fever, and seizures
20
Q

Tyramine effect

A
  • Tyramine is a naturally occurring monoamine compound that acts as a catecholamine releasing agent
  • In foods, it is often produced by decarboxylation of tyrosine during fermentation or decay

Foods containing considerable amounts of tyramine include:

    • pickled, aged, smoked, marinated, or meats that are potentially spoiled;
    • chocolate; alcoholic beverages;
    • fermented foods, such as most cheeses, etc.

Tyramine is normally metabolized by MAO; when large amounts of tyramine are ingested and MAOIs reduce metabolism, hypertensive crisis can occur – tyramine induces NE release from peripheral nerve terminals and subsequent dramatic (and potentially fatal) rise in heart rate and blood pressure

21
Q

dopamine

A

imp. in attention, motivation, pleasure, reward

** bupropion = only drug thats dopamine selective

22
Q

NE

A

imp. in alertness and energy (also seen in anxiety)

23
Q

serotonin

A

imp. in obsessions and compulsions

24
Q

Trazodone

A
  • 5-HT2 antagonist

MOA: Deceased suicidal and otherwise depressed patients have had more 5-HT2A receptors than normal patients, suggesting that postsynaptic 5-HT2A overdensity is involved in the pathogenesis of depression

ADR’s:

  • most common adverse effects are sedation and gastrointestinal disturbances
  • Sexual side effects are uncommon (priapism!)
  • Orthostatic hypotension due to α-adrenergic receptor blockade

USE: infrequently used!

25
Q

Selegiline

A

MAOI

MOA: monoamine oxidase inhibitors prevnt metabolism of NE and 5-HT and DA:
= selective irreversible MAO-B inhibitor at low doses (useful in Parkinson’s disease) and nonselective MAO-A/B inhibitor at higher doses (used to treat refractory depression)
- MAOIs cause accumulation of NE, 5-HT, and/or DA in vesicular storage in nerve endings and enhances neurotransmitter concentrations in the synaptic cleft

AE’s:

  • Orthostatic hypotension and weight gain
  • Highest rates of sexual side effects of all the antidepressants; anorgasmia is common
  • May cause dangerous interactions with certain tyramine-containing foods and with serotonergic drugs (see “Drug Interactions” below)
  • Sudden discontinuation syndrome manifested in delirium-like presentation with psychosis, excitement, and confusion
26
Q

SSRI SE?

A

NOTE:

  • Fewer side effects than older agents due to minimal affinity for muscarinic, adrenergic, and histamine receptors
  • Relatively safe in overdose unless combined with other drugs, including alcohol

SIDE EFFECTS:

  • Minor sedation and antimuscarinic side effects may occur
  • GI side effects : nausea, vomiting, upset stomach, and constipation ; may diminish after the first week of treatment
  • poor sexual function
  • Headaches, insomnia or hypersomnia, and weight gain
  • Discontinuation syndrome, causing dizziness and parethesia, can occur after sudden discontinuation of agents with short half-lives (e.g., paroxetine and sertraline)
  • Serotonin syndrome can occur with overdose or concurrent MAOI use (see “Drug Interactions” below)

CI’s: SSRIs should be discontinued or avoided in patients displaying active manic symptoms; paroxetine is contraindicated in pregnant patients

27
Q

SNRI’s AEs?

A

** have the serotonergic side effects exhibited by SSRIs but also have noradrenergic SE’s: insomnia, anxiety, and agitation (including sexual SE’s)

** Elevated blood pressure and heart rate are sometimes an issue

  • Discontinuation syndrome like that seen with SSRIs
28
Q

serotonin

A

imp. in obsessions and compulsions

29
Q

Duloxetine

A
  • SNRI

MOA: serotonin-NE reputake inhibitor : inhibit SERT and NET (NE reuptake transporter)
- no affinity for adrenergic, cholinergic or histamine rceptors = better SE profile

ADR: nausea, same SE’s as SSRIs + NE effects

30
Q

Venlafaxine

A
  • SNRI

MOA: serotonin-NE reputake inhibitor : inhibit SERT and NET (NE reuptake transporter)
- no affinity for adrenergic, cholinergic or histamine rceptors = better SE profile

AE’s: may increase the risk of bleeding via an antiplatelet aggregation effect

    • also more frequently associated with cardiac toxicity in overdose
    • dose related sustained increase in BP
31
Q

Amitriptyline

A

-TCA

MOA:inhibit SERT and NET (NE reuptake transporter)

USE: depression and pain disorders

ADR: amitriptyline exhibits marked antimuscarinic and cardiac side effects

32
Q

Desipramine

A

-TCA

USE: depression and pain disorders

MOA:inhibit SERT and NET (NE reuptake transporter)

33
Q

Imipramine

A

-TCA

MOA:inhibit SERT and NET (NE reuptake transporter)

USE: depression and pain disorders

ADR: Imipramine and amitriptyline exhibit marked antimuscarinic and cardiac side effects

34
Q

Nortriptyline

A

-TCA

USE: depression and pain disorders

MOA:inhibit SERT and NET (NE reuptake transporter)

35
Q

TCA AE’s?

A
  • Anticholinergic effects : drowsiness, dry mouth, constipation, urinary retention, blurred vision, and confusion (even w/ therapeutic doses!)
  • Orthostatic hypotension due to α-adrenergic receptor blockade, especially in the elderly
  • Weight gain and sedation due to H1 histamine receptor antagonism
  • Cardiotoxicity, arrhythmias and heart block; Convulsions; hepatic dysfunction; Hyponatremia, which may lead to confusion in the elderly
  • Hematological abnormalities (e.g., leucopenia, thrombocytopenia and agranulocytosis)
  • Sexual side effects similar to those seen with SSRIs
  • Discontinuation syndrome like that seen with SSRIs

Contraindications: Arrhythmias, recent myocardial infarction, liver disease, glaucoma, mania

36
Q

Serotonin syndrome

A

interaction of MAOIs with serotonergic agents including SSRIs, SNRIs, most TCAs, and some analgesics
- caused by overstimulation of 5-HT receptors in the central gray nuclei and the medulla

Symptoms :
- Cognitive: delirium, agitation, coma
- Autonomic: hypertension, tachycardia, hyperthermia, diaphoreses
- Somatic: myoclonus, hyperreflexia, tremor
(but no elevated CK levels, if that then think neurleptic syndrome)

** When a patient is switched from an SSRI (or other serotonergic agent) to an MAOI (or vice versa), the current therapy should be discontinued for at least 2 weeks (6 weeks for fluoxetine due to longer half-life) prior to initiation of the new therapy

Treatment: withdraw the offending drug, sedation with benzodiazepines, paralysis, intubation, and ventilation; consider 5-HT2 block with cyproheptadine or chlorpromazine

37
Q

Tyramine effect

A

d/t MAOI use

  • Tyramine is a naturally occurring monoamine compound that acts as a catecholamine releasing agent
  • In foods, it is often produced by decarboxylation of tyrosine during fermentation or decay

Foods containing considerable amounts of tyramine include:

    • pickled, aged, smoked, marinated, or meats that are potentially spoiled;
    • chocolate; alcoholic beverages;
    • fermented foods, such as most cheeses, etc.

Tyramine is normally metabolized by MAO; when large amounts of tyramine are ingested and MAOIs reduce metabolism, hypertensive crisis can occur – tyramine induces NE release from peripheral nerve terminals and subsequent dramatic (and potentially fatal) rise in heart rate and blood pressure

38
Q

no sexual side effects?

A

buproprion (SSRIs and SNRIs have a lot of problems with this!)

39
Q

TCA OD?

A

don’t give a TCA to pt. w/ suicidal risk

Three C’s: coma, cardiotoxicity, and convulsions

** Can be fatal

40
Q

bupropion

A

tetracycline/unicyclic agent

  • smoking cessation
  • less sexual dysfunction

Mechanism of Action
Incompletely understood

CNS activating properties - occasionally associated with agitation, insomnia, and anorexia

ADR’s: increased risk of seizures.

41
Q

mirtazapine

A
  • tetracyclic and unicyclic agent
  • see lots of weight gain, and increased appetite (good for depressed elderly)
  • does not cause sexual dysfunction
42
Q

mirtazapine

A
  • tetracyclic and unicyclic agent

* see lots of weight gain, and increased appetite (good for depressed elderly)

Psych: Test 1 (6 decks)

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