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Adv Pharm > Chapter 27: Antidepressants > Flashcards

Chapter 27: Antidepressants Flashcards

1
Q

depression

A

Most common psychiatric disorder ​

30% of the U.S. population will experience some form during their lifetime​

Approximately one in every eight adults in the United States is depressed​

Incidence in women twice as high as that in men​

Risk of suicide is high with depression​

Often untreated

~ 15 mil adults. 1 in every 8 in US ​

Only ~ 35% of people get treated

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2
Q

clinical features of depression

A

Depressed mood​

Loss of pleasure or interest​

Insomnia (or sometimes hypersomnia)​

Anorexia (or sometimes hyperphagia)​

Mental slowing and loss of concentration​

Feelings of guilt, worthlessness, and helplessness​

Thoughts of death and suicide​

Overt suicidal behavior​

Symptoms must be present most of the day, nearly every day, for at least 2 weeks

Grief and sadness are different that depression ​

Grief and sadness are normal responses to stressors and will resolve spontaneous

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3
Q

depression pathogenesis

A

Complex and incomplete​

Possible contributing factors:​
Genetic heritage​
Difficult childhood​
Chronic low self-esteem​

Monoamine hypothesis of depression​
Depression is caused by the functional insufficiency of monoamine neurotransmitters

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4
Q

tx for depression

A

Pharmacotherapy​
Primary therapy​

Depression-specific psychotherapy (e.g., cognitive behavioral therapy and interpersonal psychotherapy)​
Electroconvulsive therapy (somatic therapy)​
When drugs and psychotherapy have not worked​
When a rapid response is needed​
For severely depressed patients​
For suicidal patients​
For elderly patients at risk of starving​

Transcranial magnetic stimulation

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5
Q

basic considerations for depression tx

A

Time course of response​
Symptoms resolve slowly​
Initial responses develop after 1 to 3 weeks​
takes at least 4-8 wk to assess efficacy
Maximal responses may not be seen for 12 weeks​

Failure when taken 1 month without success​

Drug selection​
Antidepressants have nearly equal efficacy​
Selection​

Managing treatment

Start low dose and gradually increase ​

Ineffective- increase dose, if still ineffective can switch to mother med in same class, switch to a drug in different class, add TCA ​

After depression is treated, cont tx for 4-9 months to prevent relapse​

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6
Q

suicide risk with antidepressants

A

May increase suicidal tendencies during early treatment​

Patients should be observed closely for the following:​
Suicidality​
Worsening mood​
Changes in behavior​

Precautions​:
Prescriptions should be written for the smallest number of doses consistent with good patient management​
Dosing of inpatients should be directly observed

When meds start to work, get more motivation to suicide ​

Admin in inpatient setting should be directly observed

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7
Q

AD across lifespan

A

Infants​

Children​

Pregnant women​

Breastfeeding women​

Older adults

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8
Q

SSRI

A

Introduced in 1987​

Most commonly prescribed antidepressants​

As effective as tricyclic antidepressants (TCAs) but do not cause hypotension, sedation, or anticholinergic effects​

Overdose does not cause cardiac toxicity​

Death by overdose is extremely rare

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9
Q

Fluoxetine [Prozac, Sarafem] uses

A

SSRI -first avail

Most widely prescribed SSRI in the world​

Bipolar disorder​

Obsessive-compulsive disorder​

Panic disorder​

Bulimia nervosa​

Premenstrual dysphoric disorder​

Off-label uses: Posttraumatic stress disorder, social phobia, alcoholism, attention-deficit/hyperactivity disorder, Tourette syndrome, and obesity​

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10
Q

fluox MOA

A

Produce selective inhibition of serotonin reuptake​

Produce central nervous system (CNS) excitation

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11
Q

fluox pharmacokinetics

A

Well absorbed with PO​

Half life of 2 days –fluco​

Neurofloctine 7 day half life ​

SE sexul dysfunction and weight gain

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12
Q

fluox serotonin syndrome

A

Begins 2 to 72 hours after treatment​

Altered mental status (e.g., agitation, confusion, disorientation, anxiety, hallucinations, and poor concentration) ​

Incoordination, myoclonus, hyperreflexia, excessive sweating, tremor, and fever​

Deaths have occurred​

Syndrome resolves spontaneously after discontinuing the drug​

Risk increased by concurrent use of MAOIs and other drugs​

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13
Q

fluox drug interactions

A

Monoamine oxidase inhibitors​
Risk of serotonin syndrome​

Antiplatelet drugs and anticoagulants​

Aspirin and nonsteroidal antiinflammatory drugs​
Increase r/o bleeding​

Warfarin​
Watch INR

TCAs and lithium​
Can elevate levels of these drugs

Fluoxetine is highly bond plasma protien and compete with other drugs​

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14
Q

sertraline [zoloft]

A

Blocks uptake of serotonin and dopamine​

CNS stimulation​

Minimal effects on seizure threshold​

SSRI

If SE with one, try another. Remember to withdrawal slowly

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15
Q

sertraline uses

A

Major depression​

Panic disorder​

Obsessive-compulsive disorder​

Posttraumatic stress disorder​

Premenstrual dysphoric disorder​

Social anxiety disorder

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16
Q

sertraline SE

A

Headache ​

Nausea​

Tremor ​

Diarrhea​

Insomnia ​

Weight gain​

Agitation ​

Sexual dysfunction​

Neonatal abstinence syndrome and persistent pulmonary hypertension of the newborn when used during late pregnancy​

Nervousness​

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17
Q

sertraline drug interactions

A

MAOIs​

Pimozide

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18
Q

Fluvoxamine [Luvox]

A

Inhibition of serotonin reuptake​ SSRI

Used for obsessive-compulsive disorder​

Rapidly absorbed from the gastrointestinal tract​

Half-life: About 15 hours​

Interacts adversely with MAOIs

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19
Q

Fluvoxamine [Luvox] SE

A

Nausea​

Vomiting​

Constipation​

Weight gain​

Dry mouth​

Headache​

Sexual dysfunction ​

Abnormal liver function​

Sedative effects

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20
Q

Paroxetine [Paxil, Paxil CR, Pexeva] uses

A

Inhibition of serotonin uptake​ SSRI

Indications​

Major depression​

Obsessive-compulsive disorder​

Social phobia​

Panic disorder​

Generalized anxiety disorder​

Posttraumatic stress disorder​

Premenstrual dysphoric disorder​

Postmenopausal vasomotor symptoms

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21
Q

Citalopram [Celexa]

A

Does not block receptors for serotonin, acetylcholine, norepinephrine (NE), or histamine​

Used for major depression​

Half-life: About 35 hours​

Side effects (most common)​
Nausea​
Somnolence​
Dry mouth​
Sexual dysfunction​

Can cause neonatal abstinence syndrome​

Interacts with MAOIs

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22
Q

escitalopram [lexapro]

A

S-isomer of citalopram​

Better tolerated than citalopram​

Side effects​
Nausea​
Insomnia​
Somnolence​
Sweating​
Fatigue​

Interacts with MAOIs​

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23
Q

SNRI

A

Venlafaxine [Effexor]​

Duloxetine [Cymbalta]​

Block neural uptake of serotonin and NE. Min effects on those other transmitters ​

Similar effects to SSRIs ​

SSRI typicaly better tolerated

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24
Q

Venlafaxine [Effexor]

A

Blocks NE and serotonin uptake​

Does not block cholinergic, histaminergic, or alpha1-adrenergic receptors​

Serious reactions if combined with MAOIs​

First available ​

Well absorbed with or without food ​

Half life of 5h​

11h for active metabolite

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25
Q

Venlafaxine uses

A

Major depression​

Generalized anxiety disorder​

Social anxiety disorder (social phobia)

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26
Q

effexor SE and drug interactions

A

Nausea ​-30-50% will get nausea

Headache​

Anorexia​ -dose depend

Nervousness​

Sweating​

Somnolence ​

Insomnia​

Weight loss/anorexia​

Diastolic hypertension​

Sexual dysfunction​

Hyponatremia (in older adult patients)​

Neonatal withdrawal syndrome (late in preg)

Don’t use in glaucoma pt bc of sustained mydrasis, increased r/o eye injury​

Don’t stop abruptly ​

Don’t use with MAOI or other sertogenic drugs ​

use in combo carefully with SSRI​

MOAI should be stopped 14 days before starting effector an if switching from Effexor to MOAI –stop 7 days before​

27
Q

Desvenlafaxine [Pristiq] MOA

A

Strong inhibitor of 5-hydroxytryptamine and NE reuptake​

Does not block cholinergic, histaminergic, or alpha1-adrenergic receptors

28
Q

pristiq SE

A

Nausea ​

Headache​

Dizziness ​

Insomnia​

Diarrhea​

Dry mouth​

Sweating​

Constipation​

Sexual effects, including erectile dysfunction​

Decreased libido

29
Q

Duloxetine [Cymbalta] MOA and uses

A

Inhibits serotonin and NE reuptake​

Weakly inhibits dopamine reuptake​

Does not inhibit monoamine oxidase (MAO)​

Relieves depression​

Relieves pain of diabetic peripheral neuropathy

30
Q

Duloxetine [Cymbalta] pharakinetics

A

Well absorbed after oral administration​

Food reduces rate of absorption​

Highly bound to albumin in the blood​

Half-life: 12 hours

31
Q

Duloxetine [Cymbalta] SE

A

Nausea​

Somnolence​

Dry mouth​

Sweating​

Insomnia ​

Blurred vision​

Effects in pregnancy and lactation

32
Q

Duloxetine [Cymbalta] drug interactions

A

Alcohol​

MAOIs​

Drugs that inhibit CYP1A2 or CYP2D6

33
Q

Levomilnacipran [Fetzima]

A

New serotonin/norepinephrine reuptake inhibitor approved for major depressive disorder ​

Adverse effects​

Erectile dysfunction​

Constipation​

Nausea

34
Q

TCA

A

Drugs of first choice for many patients with major depression​

Most common adverse effects: Sedation, orthostatic hypotension, and anticholinergic effects​

Most dangerous adverse effect: Cardiac toxicity​

May increase risk of suicide during early treatment​

est 1950s

35
Q

TCA chemistry

A

Nuclei of the TCAs have three rings​

Similar to phenothiazine antipsychotics​

Produce varying degrees of the following:​
Sedation​
Orthostatic hypotension​
Anticholinergic effects

36
Q

TCA MOA

A

Block neuronal reuptake of two monoamine transmitters​

NE​

Serotonin

37
Q

pharmacokinetics TCA

A

Long and variable half-lives​

Usually single daily dose​

Requires individualization of dosage

38
Q

TCA uses

A

Depression​

Bipolar disorder​

Fibromyalgia syndrome​

Other uses
Neuropathic pain​
Chronic insomnia​
Attention-deficit/hyperactivity disorder​
Panic disorder​
Obsessive-compulsive disorder​

39
Q

TCA ADRS

A

Orthostatic hypotension​

Anticholinergic effects​

Diaphoresis​

Sedation​

Cardiac toxicity –blocks vagel influences, slows conduction at bundle of his​

Seizures​

Hypomania

suicide risk early in tx

40
Q

TCA drug interactions

A

MAOIs –r/o hypertensive crisis ​

Direct-acting sympathomimetic drugs​
poteniate​

Indirect-acting sympathomimetic drugs​
Decrease response ​

Anticholinergic agents​

CNS depressants

41
Q

TCA toxicity

A

Primarily from anticholinergic and cardiotoxic actions​

Dysrhythmias​

Tachycardia​

Intraventricular blocks​

Complete atrioventricular block​

Ventricular tachycardia​

Ventricular fibrillation

42
Q

TCA tox tx

A

Gastric lavage​

Ingestion of activated charcoal​

Intravenous sodium bicarbonate to treat cardiac dysrhythmias caused by cardiotoxicity

43
Q

TCA dosage and routes

A

Dosage​
Initial doses should be low​

Routes of administration​
All can be administered by mouth

44
Q

TCA prep and drug selection

A

All TCAs considered to be equally effective​

Selection based on side effects

45
Q

TCA considerations

A

Baseline ekg –esp of they have baseline dysrhythmias and over 40y​ and periodicallu​

Edu on ortho hypo and anticholinergic​

46
Q

MAOI

A

Second or third choice antidepressants for most patients​

As effective as TCAs and SSRIs but more hazardous​

Risk of triggering hypertensive crisis if patient eats foods rich in tyramine​

Drug of choice for atypical depression​

Isocarboxazid [Marplan]​

Phenelzine [Nardil]​

Tranylcypromine [Parnate]

takes several weeks to peak activity

47
Q

MAOI MOA

A

Convert monoamine neurotransmitters (NE, serotonin, and dopamine) into inactive products​

Inactivate tyramine and other biogenic amines​

Two forms of MAO in the body:​

MAO-A​
Inactivate NE​

MAO-B​
Inactivate dopamine​

Affected by antidepressants​

Act on MAO in two ways: reversible and irreversible​
Reversible: Lasts 3 to 5 days​
Irreversible: Lasts about 2 weeks​

All of the MAOIs in current use cause irreversible inhibition

48
Q

MAOI uses

A

Depression​

Other uses​
Bulimia nervosa​
Agoraphobia​
Attention-deficit/hyperactivity disorder​
Obsessive-compulsive disorder​
Panic attacks

49
Q

MAOI ADR

A

CNS stimulation​

Orthostatic hypotension​

Hypertensive crisis from dietary tyramine

50
Q

MAOI Hypertensive crisis/dietary tyramine

A

Tyramine: Promotes the release of NE from sympathetic neurons​

Hypertensive crisis​

Severe headache​

Tachycardia​

Hypertension​

Nausea and vomiting​

Confusion​

Profuse sweating​

Stroke ​

Death

51
Q

tyramine foods to avoid

A

Aged cheesed (cheddar, Swiss, parm, blue cheese, Gorgonzola), cured meats (suausages, pepperoni, salami), smoked or processed meats (hot dogs, corned beef, smoked fish) pickled foods (sourkrut), sauces (soy, shrimp, teriyaki), soybean products, snow pea, dried or over ripe fruits (raisins or prunes), meat tenderizers, alc (beer, red wine, sherry lqiers)

52
Q

MAOI HTN crisis tx

A

Sodium nitroprusside (a nitric oxide donor)​

Phentolamine (an alpha-adrenergic antagonist)​

Labetalol (an alpha-adrenergic and beta-adrenergic antagonist)

53
Q

MAOI drug interactions and route

A

Drug interactions​
Indirect-acting sympathomimetic agents​
Interactions secondary to the inhibition of hepatic MAO​
Antidepressants: TCAs and SSRIs​
Antihypertensive drugs​
Meperidine​

Preparations, dosage, and administration​
All MAOIs administered orally

54
Q

Selegiline [Emsam]

A

First transdermal treatment for depression​

Much lower risk of hypertensive crisis with transdermal route as compared with oral route​

Enters the system without going through the gastrointestinal tract​

Adverse effects still occur when used with sympathomimetic drugs​

Avoid carbamazepine [Tegretol] and oxcarbazepine [Trileptal]

55
Q

Bupropion [Wellbutrin]

A

Actions and uses​
Acts as stimulant and suppresses appetite​
Antidepressant effects begin in 1 to 3 weeks​
Does not affect serotonergic, cholinergic, or histaminergic transmission​
Does not cause weight gain
may increase sex drive
MDD and SAD ​
Marked as sybaritic and burden to aid in smokin cessation​
Unlabeled uses: neuropathic pain, depressive episodes in BPD, manage ADHD

56
Q

wellbutrin ADR

A

Seizures​

Agitation​

Tremor​

Tachycardia​

Blurred vision ​

Dizziness​

Headache​

Insomnia

Dry mouth​

Gastrointestinal upset ​

Constipation​

Weight loss

57
Q

well butrin drug interactions

A

MAOIs can increase the risk of bupropion toxicity

58
Q

wellbutrin admin

A

Immediate-release, sustained-release, and extended-release tablets

59
Q

other atyial AD

A

Mirtazapine [Remeron]​
Salmonella’s weight gain, elevated cholesterol levels ADR ​
Well tolerated ​

Nefazodone [Serzone]​

Trazodone [Oleptro]​

Vilazodone [Viibryd]​

Amoxapine

60
Q

nonconventional drugs for depression

A

St. John’s wort (Hypericum perforatum)​

S-adenosylmethionine

61
Q

ECT

A

Outside the realm of pharmacology​

Valuable treatment for depression​

Two desirable characteristics​
Effectiveness​
Rapid response (relative to antidepressant drugs)​

Two primary types of patients​
Those who have failed to respond to drugs​
Those who are severely depressed and suicidal​

Can terminate ongoing depressive episode​

Adverse effect​
Some loss of memory for events immediately surrounding treatment

62
Q

TMS

A

Outside the realm of pharmacology​

Reserved for severe refractory depression​

Employs an insulated magnetic coil placed against the scalp to deliver pulsed magnetic fields to the left dorsolateral prefrontal cortex​

Daily 40-minute sessions for 6 weeks ​

Adverse effects​
Transient headaches, scalp discomfort, eye pain, toothache, muscle twitching, and seizures; cognitive changes have not been reported​

63
Q

VNS

A

For long-term therapy of treatment-resistant depression​
When at least four antidepressant drugs have failed​

Mechanism of action​
An implanted device​
Delivers electrical pulses to the vagus nerve​

Side effects​
Hoarseness​
Voice alteration​
Cough​
Dyspnea

64
Q

light therapy

A

Exposure to bright light ​

Effective treatment for seasonal affective disorder and nonseasonal major depression​

May enhance serotonergic neurotransmission​

The more intense the light, the greater the response

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