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Psych Exam 1 > Antidepressants (Linger) > Flashcards

Antidepressants (Linger) Flashcards

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1
Q

SSRIs

drug list

A 
Citalopram (Celexa)
Escitalopram (Lexapro)
Fluoxetine (Prozac)
Fluvoxamine*
Paroxetine (Paxil)
Sertraline (Zoloft)
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2
Q

SNRIs

drug list

A

Duloxetine
Venlafaxine

have actions at > serotonin and norepinephrine transporters

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3
Q

Tetracyclics and Unicyclics

(atypical antidepressants) drug list

A

Bupropion
Mirtazapine (common for seniors due to depression and weight loss issues)

have potent action at NE transporters

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4
Q

5-HT Modulators

drug list

A

Trazodone - can cause priapism (erection)

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5
Q

TCAs drug list (tricyclic)

A

Amitriptyline
Desipramine
Imipramine
Nortriptyline

not first line anymore

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6
Q

MAOIs drug list

A

Selegiline

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7
Q

Biological Basis of Depression

A

Several hypotheses have been proposed

  • Monoamine Hypothesis
  • Receptor Hypothesis
  • Neurotrophic Factor Hypothesis
  • Neuroendocrine Factor Hypothesis

These hypotheses are not mutually exclusive

MDD is a complex disease likely to involve aspects of all these ideas

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8
Q

Mood is regulated by 3 systems

A

dopamine (attention, motivation, pleasure, reward)

norepinephrine (alertness, energy)

Serotonin (obsessions and compulsions)

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9
Q

Major Classes of Antidepressants

A

First-line agents:

  • Selective Serotonin Reuptake Inhibitors (SSRIs)
  • Serontonin-Norepinephrine Reuptake Inhibitors (SNRIs)
  • (Some) Tetracyclics and Unicyclics (catch-all class)

Second- and third-line agents:

  • Tricyclic Antidepressants (TCAs)
  • Monoamine Oxidase Inhibitors (MAOIs)

Infrequently used agents:
- 5-HT2 Antagonists

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10
Q

Efficacy of Antidepressants

A

30-40% of patients achieve remission within a single trial of 8-12 weeks
70-80% of patients achieve remission by switching to another agent or augmentation by addition of another drug
* Antidepressant drugs are roughly equivalent in terms of efficacy
Antidepressants are more effective when combined with psychotherapy

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11
Q

Choosing an Antidepressant

A

The choice of an antidepressant depends first on the indication; not all indications are equally responsive to all antidepressants
In the treatment of MDD, safety and side effects are usually primary considerations in deciding which drug will be tried first in a depressed patient
Although antidepressant drugs are roughly equivalent in terms of efficacy, individual patients may fare better on one drug than on another for unknown reasons
Often finding the right drug for a patient must be done by trial and error

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12
Q

Selective Serotonin Reuptake Inhibitors (SSRIs)

A

Newest generation of antidepressants
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

Fluoxetine (Prozac®)
Sertraline (Zoloft®)
Paroxetine (Paxil®)
Citalopram (Celexa®)
Escitalopram (Lexapro®)
Fluvoxamine* (Luvox®)
  • Labeled only for obsessive-compulsive disorder
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13
Q

SSRIs: Mechanism of Action

A

Allosteric inhibition of the serotonin transporter (SERT)
Effectively increases the concentration of serotonin in the synaptic cleft
~80% of SERT activity is blocked at therapeutic doses
Downregulation of postsynaptic 5-HT2A receptor density has been proposed as an adaptive process provoked by chronic administration of SSRIs

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14
Q

SNRIs & TCAs: Mechanism of Action

A

Inhibit SERT and NET, the norepinephrine reuptake transporter
Effectively increases the concentration of both 5-HT and NE in the synaptic cleft
Most SNRIs tends to exhibit greater affinity for SERT than for NET
Different TCAs have different relative affinities for either NET or SERT

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15
Q

MAOIs: Mechanism of Action

A

MAOs are mitochondrial enzymes that metabolizes monoamines
MAOIs cause accumulation of NE, 5-HT, and/or DA in vesicular storage in nerve endings and enhances neurotransmitter concentrations in the synaptic cleft

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16
Q

5-HT2 Antagonists: Mechanism of Action

A

5-HT2A receptor inhibition is associated with substantial antianxiety, antipsychotic, and antidepressant effects
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

Trazodone: rare ADR = priapism

17
Q

SSRIs: Common Side Effects

A

Sexual dysfunction occurs in 30-40% of patients
GI disturbances
Initial agitation and insomnia
Sedation – usually less frequent than seen with TCAs

Discontinuation syndrome, causing dizziness and parethesia (feeling of “pins and needles”), can occur after sudden discontinuation of agents with short half-lives (e.g., paroxetine and sertraline)

18
Q

Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs)

A

Duloxetine (Cymbalta®)

  • Nausea is a significant side effect
  • Taper up and down slowly to avoid side effects

Most SNRIs exhibit the same side effects as SSRIs (e.g., sexual side effects) as well as noradrenergic effects

Venlafaxine (Effexor®)

  • Low sedative and antimuscarinic effects
  • Dose-related, sustained increase in blood pressure
  • – Particularly problematic in overdose (cardiac toxicity)
  • – Potentially dangerous with abrupt discontinuation
19
Q

Bupropion: A Unicyclic Agent

A

CNS activating properties - occasionally associated with agitation, insomnia, and anorexia; lowers seizure threshold

Little or no sexual dysfunction

Mechanism of action incompletely understood

  • Selective inhibitor of the dopamine transporter (DAT) and stimulates presynaptic release of NE and DA
  • Virtually no direct effect on serotonin reuptake or receptors

Also used in smoking cessation

  • Inhibitor of neuronal nicotinic receptors
  • Marked under different trade name (Zyban)
20
Q

Tricyclic Antidepressants (TCAs)

A

Were the dominant class of antidepressants until the introduction of SSRIs

Highly effective, but exhibit numerous side effects due to high affinity for muscarinic receptors, H1 histamine receptors, and α-adrenergic receptors

Amitriptyline (Elavil®)
- Has the most sedative and strongest antimuscarinic and cardiac side effects of all the TCAs

21
Q

TCAs: Dangerous in Overdose!

A

A patient may overdose on as little as a 4 day supply of TCAs (depressed patients are at risk for suicide)

The three Cs: coma, cardiotoxicity, and convulsions

Can be fatal

The pharmacokinetics of TCAs hinder treatment of overdose (large volume of distribution and high plasma protein binding make dialysis ineffective in removing ingested drug)

  • MAOIs are also potentially lethal in overdose producing autonomic instability, hyperadrenergic symptoms, psychotic symptoms, confusion, delirium, fever, and seizures
22
Q

MAOIs: Serotonin Syndrome

A

Life-threatening interaction of MAOIs with serotonergic agents including SSRIs, SNRIs, most TCAs, and some analgesics
Thought to be caused by overstimulation of 5-HT receptors
Symptoms range from mild to lethal: sweating, rigidity, hyperthermia, autonomic instability, seizures
Discontinue for two weeks before switching drug classes

23
Q

Monoamine Oxidase Inhibitors (MAOIs)

A

First used about the time of the TCAs (mid 1950’s)

Generally as effective as other antidepressants

Rarely used because of the risk of interactions with many foods (those high in tyramine) and drugs (sympathomimetic agents)

Isocarboxazid
Phenelzine 
Selegiline 
Tranylcypromine 
Side effects
Orthostatic hypotension and weight gain
Highest rates of sexual side effects of all the antidepressants
24
Q

MAOIs: Tyramine Interactions

A

Tyramine is a naturally occurring monoamine compound that stimulates catecholamine release
In foods, it is often produced by decarboxylation of tyrosine during fermentation or decay
Tyramine is normally metabolized by MAO
When MAOIs reduce tyramine metabolism, hypertensive crisis can occur – dramatic (and potentially fatal) rise in heart rate and blood pressure

Foods to avoid:
Pickled, aged, or smoked meats and fish
Chocolate
Beer and wine
Aged cheeses
Fava beans
Dried sausages
Yeast extract
And others
25
Q

Drug Drug interactions

A

TCAs are metabolyzed by CYP enzymes

Fluvocamine, fluoxetine are inhibitors

tobacco, rifampin, phenobarbital, barbiturates, glucocorticoids are inducers

26
Q

Clinical Indications: Anxiety Disorders

A

After MDD, most common use of antidepressants
Many SSRIs and SNRIs are approved for all the major anxiety disorders
May be more effective than benzodiazepines for treating anxiety disorders and do not carry the associated risks of dependence and tolerance
OCD is known to respond to serotonergic agents, especially fluoxetine, fluvoxamine, paroxetine, and clomipramine

Post-traumatic stress disorder (PTSD)
Obsessive-compulsive disorder (OCD)
Social anxiety disorder
Generalized anxiety disorder (GAD)
Panic disorder
27
Q

Clinical Indications: Pain Disorders

A

Antidepressants possess analgesic properties independent of their mood effects
Chronic pain conditions are also commonly associated with depression
TCAs have been used in the treatment of neuropathic and other pain conditions since the 1960s; SNRIs are also increasingly used
Some trials suggest that SSRIs are less effective, possibly due to key roles of both NE and 5-HT in pain disorders

28
Q

Other Clinical Indications

A 
Premenstrual Dysphoric Disorder
- SSRIs fluoxetine and sertraline
Smoking Cessation – Bupropion
Premature ejaculation – SSRIs
Bulimia nervosa – fluoxetine and other SSRIs
Insomnia – amitriptyline and trazodone
Enuresis – TCAs
29
Q

We start a patient with depression on a drug that selectively inhibits neuronal 5-HT reuptake and has minimal effect on the reuptake of NE or DA. Which drug belongs to a class that best fits this description?

Amitriptyline
Bupropion
Fluoxetine
Imipramine
Venlafaxine
A

Fluoxetine is the SSRI.

30
Q

In deciding on pharmacotherapy for many patients you’ve diagnosed with depression, you’ve usually considered starting with an SSRI or, in some cases, a tricyclic. Today you assess a patient and suspect endogenous depression. While discussing treatment options they refer to a drug by name and ask you about it; they’ve seen it advertised on TV. The drug is bupropion (Wellbutrin). In what main way does bupropion differ from the SSRIs and TCAs?

Higher incidence of CNS depression, drowsiness
Higher incidence of weight gain
Less drug-induced sexual dysfunction
More common and severe falls of resting blood pressure
More severe and frequent antimuscarinic effects

A

Less drug-induced sexual dysfunction

31
Q

One reason for the declining use of tricyclic antidepressants such as imipramine, and the growing use of newer classes, is the prevalence of common tricyclic-induced side effects or adverse responses. What side effect or adverse response is most likely to occur with the usual therapeutic doses of a tricyclic?

Antimuscarinic effects
Arrhythmias
Hepatotoxicity
Nephrotoxicity
Seizures
A

Antimuscarinic effects

32
Q

A 31-year-old woman has been treated with fluoxetine for 5 months. She is diagnosed with another medical problem and receives one or more drugs that would otherwise be suitable and probably problem-free. She is rushed to the ED with unstable vital signs, muscle rigidity, myoclonus, CNS irritability, altered consciousness, and shivering. What add-on drug(s) most likely caused these responses?

Codeine for cough
Loratadine for seasonal allergies
Midazolam and fentynyl, used to ease discomfort from endoscopy
Sumatriptan for migraine
Zolpidem for short-term insomnia
A

Sumatriptan for migraine

- serotonin syndrome (this is a serotonin agonist)

Psych Exam 1 (17 decks)

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