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Advanced Pharmacology > Antidepressant Agents > Flashcards

Antidepressant Agents Flashcards

1
Q

Lifetime prevalence of depression in men and women:

A

-10-25% of women
-5-10% of men

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2
Q

___-___% of diagnosed individuals receive treatment for depression, and 25% of those who recieve treatment get adequate treatment

A

25-50

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3
Q

Average age of onset of depression is late ____

A

20s

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4
Q

Depression usually lasts ___-___ if untreated and also has a release risk

A

6 months-2 years

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5
Q

____ is prevalent in those who are depressed; an estimated 8-25 attempts occur per every suicide death

A

Suicide

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6
Q

In 2004, suicide was the ____ leading cause of death in those aged 10-14, 15-19, and 20-24

A

3rd

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7
Q

In May of 2007, the FDA extended a warning of SSRI to young adults aged ___-___

A

19-24

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8
Q

It is now estimated that ____% of adults with depression do not receive antidepressant therapy (no compensatory increases in other pharmacotherapies) (prior to the warning, 20% did get treatment)

A

30

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9
Q

What are types of unipolar depression?

A

-Major depressive disorder
-Dysthymia
-Double depression
-Psychotic depression (not the same as depression secondary to schizophrenia)
-Seasonal affective disorder
-Postpartum depression

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10
Q

What are examples of depression symptoms?

A

-Sleep patterns altered
-Interests gone
-Guilt
-Energy or fatigue
-Concentration/memory problems
-Appetite increased or decreased
-Psychomotor changes: agitation or retardation
-Suicidal thoughts; thoughts of death

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11
Q

“Too much” neurotransmission means that hyperexcitable neurons fire in the absence of appropriate stimuli, like with ____ disorders

A

Seizure

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12
Q

When too many neurotransmitters bind to postsynaptic receptors, it causes ____

A

Psychosis

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13
Q

When too few neurotransmitters bind to postsynaptic receptors, it can lead to things like…

A

-Depression
-Parkinson’s disease
-ADHD

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14
Q

The monoamine hypothesis of depression says that depression is caused by a functional insufficiency of the monoamine neurotransmitters ____, ____, or both

A

Norepinephrine, serotonin

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15
Q

There may also be a deficiency in ____ with depression

A

Dopamine

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16
Q

What are the goals of antidepressant drugs?

A

-Increase neurotransmitter synthesis or release
-Prolong time of the neurotransmitter in the synapse
-Inhibiting the enzymes that degrade neurotransmitters
-Administering agonists that act at post-synaptic receptors

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17
Q

What impacts the “nurture” pathophysiology of depression?

A

-Stress and hypothalamic-pituitary axis
-Childhood neglect

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18
Q

What impacts the “nature” pathophysiology of depression?

A

-Genetics
-Environmental exposure

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19
Q

Observations made in the 1950s of the effects of ____ and ____ in altering monoamine neurotransmitter levels and affecting depressive symptoms gave indications of the pathophysiology of depression

A

Reserpine and isoniazid

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20
Q

What is the process of neuronal transmission?

A

-Action potential reaches of synapse
-Neurotransmitter is released and interacts with post-synaptic receptors
-Neurotransmitter action is terminated by “reuptake” pumps that rapidly remove neurotransmitter from the synapse
-Monoamine oxidase (MAO) metabolized excess neurotransmitter in terminal preventing accumulation

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21
Q

Selecting manipulation of the ____ transmitters (dopamine, serotonin, norepinephrine) has been the common denominator for all the currently marketed antidepressants (the same systems are implicated in anxiety)

A

Aminergic

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22
Q

Most currently availble drugs increase monoamine mediated neurotransmission in key areas of the limbic system that regulate…

A

-Mood
-Arousal
-Appetite
-Sleep

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23
Q

General mechanism of increasing monoamine neurotransmission include increasing the ___ ___ ___

A

Synaptic residence time

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24
Q

What are two mechanisms to increase synaptic residence time?

A

-Blocking the reuptake of norepinephrine, serotonin, and dopamine into nerve terminals
-Blocking the metabolism of norepinephrine and serotonin in nerve terminals (MAOIs)

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25
Q

Antidepressants selectively alleviate symptoms of depression rather than acting as general ___ ___

A

CNS stimulants

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26
Q

Neurotransmitter levels in the synapse ____ soon after administration of most antidepressants, yet alleviation of depression is slow (weeks)

A

Increases

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27
Q

Stopping the antidepressant agent suddenly will result in rapid ____ of neurotransmitters

A

Release

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28
Q

One course of pharmacotherapy for depression is approximately ___ ___ long

A

1 year

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29
Q

Antidepressant medications do not work for everyone; about ____% of people are considered non-responders

A

30

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30
Q

The treatment goal in the acute phase of depression is to…

A

-Reduce and eliminate symptoms

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31
Q

The treatment goal in the continuation phase is to…

A

-Prevent relapse and return of symptoms

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32
Q

The treatment goal of the maintenance phase is to…

A

-Protect susceptible patients against recurrence of future depressive episodes

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33
Q

What are some examples of nonpharmacological treatment options for depression?

A

-Psychotherapy
-Phototherapy and chronotherapy
-Electroconvulsive therapy
-Vagal nerve stimulation
-Transcranial magnetic stimulation

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34
Q

What are examples of pharmacological treatment options for depression?

A

-MAOIs
-TCA
-SSRI, SNRI, NRI
-Other (trazadone, nefazodone, bupropion, mirtazapine, venlafaxine, duloxetine)

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35
Q

The choice of antidepressant depends on…

A

-Previous response to pharmacotherapy
-Concomitant medications and disease states
-Tolerance of specific adverse effect profile
-Potential for suicide
-Need for multiple treatment effects
-Lifestyle considerations and cost

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36
Q

Patients who discontinue a prescription prior to 1 year of appropriate pharmacotherapy are ___ more likely to relapse within 1 year

A

2

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37
Q

Who might receive a lifelong prescription for an antidepressant?

A

-2+ episodes + family history + additional diagnosis
-3+ episodes

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38
Q

A pharmacologic ____ is seen when there is adequate dosage for adequate time period

A

Response

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39
Q

Early response can be seen in 2-3 weeks, but can often take ___-___ weeks

A

4-6

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40
Q

If there is no evidence of response in 2-3 weeks at the top dose, switch to a new ___

A

Drug

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41
Q

Often, patients are considered to be “____ ____” even though they have never had even one antidepressant titrated to the top dosage for long enough to work

A

Treatment resistant

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42
Q

____ are first line antidepressants for most patients

A

SSRIs

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43
Q

SSRIs block the presynaptic reuptake of ____

A

Serotonin

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44
Q

The observed therapeutic effect of SSRIs is delayed by several ____

A

Weeks

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45
Q

Adverse effects of SSRIs are apparent within the first ____

A

Week

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46
Q

With SSRIs, there is a ____ over-dose potential

A

Lower

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47
Q

What are some examples of available SSRIs?

A

-Fluoxetine (Prozac)-> first SSRI approved
-Sertraline (Zoloft)
-Fluvoxamine (Luvox)
-Paroxetine (Paxil)
-Citalopram (Celexa)
-Escitalopram (Lexapro)
-Vilazodone (Viibryd)

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48
Q

SSRIs are no more effective than TCAs, but they have a more favorable ___-___ profile

A

Side effect

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49
Q

SSRIs have little or no affinity for muscarinic acetylcholine, a1-adrenergic and histamine H1 receptors, therefore have more favorable side effect profile; decreased anticholinergic activity = less ____

A

Cardiotoxicity

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50
Q

Most SSRIs are administered in the ____ (since they may cause insomnia)

A

Morning

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51
Q

____ is the only SSRI that would be given at bedtime since it is sedating

A

Paroxetine

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52
Q

SSRIs have a delayed ____, but it may be somewhat less than with TCAs

A

Efficacy

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53
Q

SSRIs have an ____ effect of blocking 5-HT (serotonin) reuptake into nerve terminals

A

Immediate

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54
Q

A delayed effect of SSRIs is ____ changes in the CNS

A

Adaptive

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55
Q

What adaptive changes in the CNS can SSRIs cause?

A

-Desensitization of 5-HT1A (serotonin) autoreceptors on serotonin terminals (inhibition of serotonin release when activated)
-Desensitization of 5-HT1A (serotonin) autoreceptors on serotonin neurons (negative feedback on firing activity when activated)

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56
Q

The end result of the mechanism of SSRIs is long-term ____ of serotonin neurotransmission

A

Increase

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57
Q

SSRI adverse side effects:

A

-GI disturbances (nausea, diarrhea, cramping, heartburn)
-CNS excitation or stimulation (restlessness, insomnia, anxiety; sedation from paroxetine)
-Significant anorexia and weight loss during early treatment; possible weight gain with long-term use
-Decreased libido and significant sexual dysfunction (anorgasmia, ejaculatory delay, impotence)
-Withdrawal syndrome has been described that includes nausea, dizziness, anxiety, tremor, and palpitations

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58
Q

SSRIs undergo metabolism in the ____

A

Liver

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59
Q

Choosing among SSRIs is primarily related to differences in…

A

-Half-life
-Inhibition of cytochrome p450
-Other drugs being used

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60
Q

In general, SSRIs inhibit what enzyme of CYP450?

A

-2D6

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61
Q

SSRIs can cause elevated concentrations of drugs metabolized by 2D6; this is important for drugs with a narrow ____ ____ like TCAs or type IC antiarrhythmics

A

Therapeutic index

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62
Q

____ is an SSRI that inhibits its own metabolism and exhibits nonlinear kinetics

A

Paroxetine

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63
Q

_____ is an SSRI that has the most drug-drug interactions due to its effect on so many CYP450 enzymes

A

Fluoxetine (Prozac)

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64
Q

____ and ____ have the least amount of drug-drug interactions

A

Citalopram (Celexa); Escitalopram (Lexapro)

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65
Q

There are numerous potential drug interactions with SSRIs due to inhibition of other drugs by ____ enzymes

A

CYP450

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66
Q

SSRIs taken with monoamine oxidase inhibitors can cause ___ ___

A

Serotonin syndrome

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67
Q

What are symptoms of Serotonin Syndrome?

A

-Rapid mental status changes
-Seizures
-Coma
-Death

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68
Q

Lexapro (Escitalopram) contains only the ____-enantiomer of Celexa (citalopram)

A

S

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69
Q

The S-enantiomer is therapeutically ____, while the R-enantiomer is not

A

Active

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70
Q

Lexapro (escitalopram) is more ____ with less side effects than Celexa

A

Potent

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71
Q

Lexapro ____ mg produces the same efficacy as ____ mg of Celexa

A

10; 40

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72
Q

What are other clinical uses for SSRIs?

A

-Generalized anxiety disorder
-Social phobia
-Panic disorder
-OCD
-Bulimia Nervosa
-Migraine headache
-PMDD
-PTSD
-Seasonal affective disorder
-Post-partum depression

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73
Q

What are symptoms of SSRI withdrawal?

A

-Flu-like symptoms, malaise
-Dizziness
-GI effects
-Parasthesia
-Mood, appetite, and sleep changes

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74
Q

____ withdrawal is a problem with drugs like amitriptyline, protriptyline, imipramine, etc

A

Anticholinergic

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75
Q

We can ____ taper doses to minimize withdrawal effects of antidepressants

A

Gradually

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76
Q

Serotonin syndrome is a pharmacodynamic interaction caused by over-potentiation of serotonin effects that can cause side effects like…

A

-Cramping
-Diarrhea
-Tremor
-Restlessness
-Tachycardia
-Hypertension
-Mania symptoms
-Confusion
-Sweating

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77
Q

Serotonin syndrome can be caused by the interaction of SSRIs with…

A

-Triptains
-Buspirone
-Amphetamines
-Muscle relaxants
-MAOIs

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78
Q

What are some examples of atypical antidepressants?

A

-Buproprion (Wellbutrin)
-Trazodone (Desyrel)
-Venlafaxine (Effexor)
-Mirtazapine (Remeron)
-Nefazodone (Serzone)
-Duloxetine (Cymbalta)

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79
Q

Bupropion (Wellbutrin) has a unique mechanism of action; it works by weakly blocking the reuptake of ____, and possibly causing some blockage of the norepinephrine and serotonin reuptake

A

Dopamine

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80
Q

There are three formulations of Bupropion (Wellbutrin) available for depression as well as a form called _____ that is approved for smoking cessation

A

Zyban

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81
Q

Bupropion (Wellbutrin) is well tolerated due to little or no ____, ____, or ____ receptor effects

A

Muscarinic, alpha-adrenergic, or histaminic

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82
Q

There is ____ incidence of sedation, hypotension, and weight gain with Bupropion (Wellbutrin)

A

Low

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83
Q

Unlike other antidepressants, Bupropion (Wellbutrin) causes few ____ side effects

A

Sexual

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84
Q

Bupropion (Wellbutrin) may cause ___, ___, and ___ since it is structurally similar to amphetamine, or precipitate psychotic episodes in susceptible individuals

A

Restlessness, insomnia, anxiety

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85
Q

There is a high risk of ____ activity with Bupropion at doses of 450 mg/day (should be given in divided doses)

A

Seizure

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86
Q

What are some drug interactions with Bupropion (Wellbutrin)?

A

-Contraindicated with MAOIs
-Caution with drugs that affect CYP3A4 or CYP2D6 (Ritonavir-> Norvir, Kaletra)
-Caution with drugs that low seizure threshold (Clozapine, illicit drugs)

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87
Q

Bupropion (Wellbutrin) is contraindicated in patients with…

A

-Seizure disorders
-Bulimia or anorexia nervosa

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88
Q

What is the mechanism of action of Trazodone (Desyrel)?

A

-Blocks 5-HT (serotonin) reuptake; antagonist at 5-HT2 receptors
-Partial agonist at 5-HT1A receptors
-Litter effect on norepinephrine uptake, but may stimulate norepinephrine release

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89
Q

Side effects of Trazodone (Desyrel):

A

-Sedation: low dose used for insomnia
-GI upset (nausea and vomiting)
-Dry mouth, blurred vision
-Orthostatic hypotension
-Priapism (sustained erection)-> rare but serious

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90
Q

What is the mechanism of action of Venlafaxine (Effexor)?

A

-Blocks reuptake of norepinephrine and serotonin
-Weakly inhibits dopamine reuptake
-Little to no effect on muscarinic, adrenergic, or histaminic receptors

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91
Q

Venlafaxine (Effexor) works like an _____ at lower doses (<200 mg/day)

A

SSRI

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92
Q

There is a ____ dosing conversion from Effexor to Effexor XR

A

Direct

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93
Q

The XR formulation of Venlafaxine (Effexor) has increased ____ and may decrease GI side effects

A

Complicance

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94
Q

Side effects of Venlafaxine (Effexor):

A

-Restlessness and insomnia
-Nausea and vomiting
-Sexual dysfunction
-Increase in blood pressure in approximately 5% of patients (dose-dependent, >300 mg/day)

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95
Q

There are minimal drug interactions with Venlafaxine (Effexor); some potential for interaction with agents that are metabolized by ____ like Clozapine and Paroxetine

A

CYP2D6

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96
Q

What should be included in patient counseling for Venlafaxine (Effexor)?

A

-Avoid use with alcohol
-May cause drowsiness and coordination impairment
-Take with food
-Do not crush or chew XR capsules

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97
Q

What is the mechanism of action of Mirtazapine (Remeron)?

A

-Antagonist of central presynaptic alpha2-adrenergic receptors (increases norepinephrine and serotonin release)
-Blockade of 5-HT2 and 5-HT3 receptors

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98
Q

Mirtazapine (Remeron) is ___-___, so it only requires 1 daily administration (preferably at bedtime)

A

Long-acting

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99
Q

Clearance of Mirtazapine (Remeron) is decreased in both ____/____ impaired patients and the elderly

A

Renally/hepatically

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100
Q

Side effects of Mirtazapine (Remeron):

A

-Sedation: blockade of histamine receptors, dose at bedtime
-Significant weight gain, increased appetite and serum lipids

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101
Q

Drug interactions with Mirtazapine (Remeron):

A

-Allow 14 days between stopping an MAOI and starting Mirtazapine (Remeron) and vice versa
-Alcohol/benzodiazepines increase sedation

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102
Q

Nefazodone (Serzone) is structurally analogous to ____

A

Trazodone

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103
Q

Mechanism of action of Nefazodone (Serzone):

A

-Blocks 5-HT reuptake
-Acts as an antagonist at 5-HT2 receptors
-Partial agonist at 5-HT1A

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104
Q

Side effects of Nefazodone (Serzone):

A

-Nausea, constipation
-Blurred vision
-Less sedation and orthostatic hypotension than trazodone
-Not associated with weight gain, priapism, or sexual side effects

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105
Q

What is the black box warning on Nefazodone (Serzone)?

A

Potential life-threatening liver failure

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106
Q

Drug interaction with Nefazodone (Serzone):

A

-Inhibits CYP3A4 = many potential drug interactions (antihistamines, benzodiazepines, digoxin, etc)

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107
Q

Duloxetine (Cymbalta) was the first drug approved for the treatment of ___ ___ ___

A

Diabetic peripheral neuropathy

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108
Q

Mechanism of action of Duloxetine (Cymbalta):

A

-Inhibits the reuptake of both norepinephrine and serotonin

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109
Q

Side effects of Duloxetine (Cymbalta):

A

-Nausea
-Dry mouth
-Fatigue
-Insomnia

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110
Q

What are some examples of traditional tricyclic antidepressants (TCAs)?

A

-Imipramine (Tofranil)
-Desipramine (Norpramin, Pertofrane)
-Amitriptyline (Elavil)
-Protriptyline (Vivactil)
-Nortriptyline (Aventyl, Pamelor)
-Doxepin (Adapin, Sinequan)

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111
Q

The precise mechanism of TCAs is ____

A

Unknown

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112
Q

TCAs immediately block the reuptake of ___ ____ (both norepinephrine and serotonin) to varying degrees

A

Monoamine neurotransmitters

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113
Q

Neurotransmitter levels in the synaptic cleft increase, but the clinical effects are delayed around ___-___ weeks

A

2-3

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114
Q

It takes about 2-3 weeks for the increased neurotransmitter levels in the synapse to alter post-synaptic receptor ____ or ____

A

Density or sensitivity

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115
Q

TCAs are generally well absorbed orally, undergo high ___-___ metabolism, and are highly protein bound

A

First-pass

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116
Q

TCAs have long half-lives, which allow for once-daily dosing, generally at ____

A

Bedtime

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117
Q

TCAs are inactivated by ____ metabolism

A

Hepatic

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118
Q

TCAs undergo ____ formation of active metabolites

A

Oxidative

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119
Q

TCAs can also be conjugated with ____ ____ and excreted

A

Glucuronic acid

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120
Q

Blood levels measurements of TCAs must include the ___ ___ and ___ ___

A

Parent drug and active metabolites

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121
Q

TCAs lost their place as first-line therapy due to ___ ___, which vary in degree with any particular TCA

A

Side effects

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122
Q

Side effects of TCAs are mostly related to the blockade of…

A

-Acetylcholine receptors
-Histamine receptors

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123
Q

The blockade of acetylcholine receptors causes what side effects?

A

-Sedation
-Dry mouth
-Blurred vision
-Constipation
-Urinary retention
-Cognitive impairment

124
Q

The blockade of histamine receptors causes…

A

-Fatigue
-Sedation
(especially with initial therapy)

125
Q

Despite the lag in ____ effects with TCAs, side effects may occur immediately

A

Therapeutic

126
Q

At therapeutic doses, what side effects may be seen with TCAs?

A

-Weight gain
-Some sexual dysfunction
-Lowers seizure threshold

127
Q

At toxic doses, what effects may be seen with TCAs?

A

-Cardiovascular toxicity (Conduction delays, arrhythmias)
-Severe anticholinergic effects
-Convulsions

128
Q

TCAs have multiple possible drug _____ due to high protein binding

A

Interactions

129
Q

TCAs can be displaced by other highly protein-bound drugs like…

A

-Phenytoin
-Aspirin
-Phenothiazines

130
Q

TCA metabolism can be inhibited by…

A

-Antipsychotics
-Oral contraceptives
-SSRIs

131
Q

TCAs have a ____ therapeutic range with dose-related toxicities

A

Narrow

132
Q

___-___% of patients have insufficient enzymes to metabolize TCA drugs; this may lead to life-threatening toxicities

A

3-5

133
Q

It is important to monitor ____-____ serum drug levels of TCAs by drawing levels 10-12 hours after last dose

A

Steady-state

134
Q

_____ is the most sedating TCA, best used for patients with insomnia or excitation

A

Amitriptyline (Elavil)

135
Q

____ and ____ are TCAs that are the most effective in counteracting motor retardation

A

Nortriptyline (Pamerlor) and Desipramine (Pertofrane)

136
Q

_____ is a TCA that has antidepressant and anti-anxiety effects, therefore, it is useful when depression and anxiety are co-morbid

A

Doxepin (Adapin, Sinequan)

137
Q

_____ is a TCA that has dopamine (DA2) antagonist activity in addition to reuptake blockade; it is marketed for treatment of obsessive-compulsive disorders

A

Clomipramine (Anafranil)

138
Q

_____ is a TCA that is a metabolite of an antipsychotic drug; it may produce extrapyramidal symptoms similar to other antipsychotic drugs due to the blockade of dopamine receptors

A

Amoxapine (Ascendin)

139
Q

The function of MAO in nerve terminals is to convert ____ ____ into inactive products

A

Monoamine neurotransmitters

140
Q

MAO inhibitors potentiate monoaminergic neurotransmission by augmenting ___, ___, and ___ levels in nerve terminals

A

Norepinephrine, serotonin, and dopamine

141
Q

Inhibition of MAO is _____; termination of pharmacological activity requires discontinuance of the drug and synthesis of new enzyme that takes about 2-3 weeks

A

Irreversible

142
Q

Traditional MAOIs were _____ (meaning that they inhibited MAO-A and MAO-B) and irreversible

A

Nonselective

143
Q

What are three examples of MAOIs?

A

-Phenelzine (Nardil)
-Tranylcypromine (Parnate)
-Isocarboxazid (Marplan)

144
Q

____-____ MAO inhibitors are currently being developed and tested in clinical trials

A

Shorter-acting

145
Q

Moclobemide (Manerix) is a shorter-acting MAOI that is being tested; it is a reversible, selective inhibitor of ____ with fewer side effects with less danger of food interactions

A

MAO-A

146
Q

____-____ interactions severely limit the use of MAOI (usually agents of last choice)

A

Food-drug

147
Q

Hepatic and intestinal MAO serve to inactive biogenic amines in food (______), as well as biogenic amines administered as drugs (in decongestants)

A

Tyramine

148
Q

MAO inhibitors block the metabolism of tyramine, which could lead to a ____ ____ if a someone has a high intake of tyramine

A

Hypertensive crisis

149
Q

MAOIs tend to produce ____, along with many typical
“tricyclic” side effects

A

Insomnia

150
Q

What are other side effects of MAOIs?

A

-Dizziness
-Blurred vision
-Weight gain
-Urinary hesitancy
-Serotonin Syndrome when combined with SSRI or overdose

151
Q

_____ is an MAOI that was approved for treatment of Major Depressive Disorder in 2003

A

EmSam (Selegiline transdermal)

152
Q

EmSam (Selegiline transdermal) is _____ and inhibits both MAO-A and MAO-B enzymes in the central nervous system, while avoiding inhibition of intestinal or liver MAO-A enzymes

A

Nonselective

153
Q

EmSam is different from other MAOIs because it does not require someone to have any ___ restrictions

A

Dietary

154
Q

The onset of effect of EmSam is just a few ____

A

Days

155
Q

EmSam has excellent ____ rates and side effect profile

A

Compliance

156
Q

____ ____ major depressive disorder means that there has been no improvement after 2+ full courses of monotherapy regimens

A

Treatment-refractory

157
Q

With “treatment-refractory” major depressive disorders, it is important to see if drugs were dosed for ____ enough with adequate dosage

A

Long

158
Q

What are options for those with treatment-refractory major depressive disorder?

A

-Switching monotherapy
-Augmentation therapy
-Non-pharmacologic strategies

159
Q

What are some examples of non-Rx treatment options for refractory MDD?

A

-Psychotherapy modalities
-Phototherapy
-Transcranial magnetic stimulation therapy (TMS)
-Electroconvulsive therapy (ECT)
-Vagal nerve stimulation therapy (VNS)

160
Q

Bipolar disorder affects 2.5 million people in the United States, and symptoms can begin as early as ___-___ years old

A

5-6

161
Q

The mean age of onset of bipolar disorder is in the late ___-___, but symptoms may be more evident between ages 40-50 years old

A

20-30

162
Q

Prevalence of bipolar disorder is equal in ___ and ___

A

Men and women

163
Q

Someone is at a higher risk of developing bipolar disorder if they have family members with…

A

-Depression (90%)
-OCD
-Substance abuse

164
Q

What are examples of mood disorders?

A

-Major depressive disorder
-Dysthymic disorder
-Bipolar I disorder
-Bipolar II disorder
-Cyclothymic disorder
-Bipolar disorder NOS

165
Q

____ ____ ____ is the most common presentation of bipolar disorder

A

Bipolar II Depression

166
Q

Patients with _____ episodes are typically elated and adaptive, while ____ patients often lack specific recall of these episodes (this may result in misdiagnosis of unipolar depression)

A

Hypomanic; depressed

167
Q

With bipolar depression, someone has ____ episodes that alternate with episodes of ____; these episodes may last several weeks to months

A

Manic; depression

168
Q

____ cycling of bipolar disorder means that someone has more than 4 cycles of either depression or mania per year

A

Rapid

169
Q

Patients with bipolar disorder will often need to be managed with more than one medication; only ____% of patients respond to more than one mood stabilizer

A

30

170
Q

Symptoms of hypomania and mania:

A

-Exaggerated optimism
-Decreased need for sleep
-Grandiose delusions
-Inflated sense of self-importance
-Excessive irritability
-Increased mental or physical activity
-Racing speech; flight of ideas
-Impulsiveness, poor judgment, reckless behavior
-Easy distracted
-Psychosis

171
Q

Mania usually begins with changes in ____ ____; symptoms gradually develop over three days in three stages

A

Sleep patterns

172
Q

Stage 1 of episode development is hypomania; this includes symptoms like…

A

-Racing thoughts
-Liable affect
-Grandiosity
-Increased activity/speech

173
Q

Stage 2 of episode development is mania; this includes symptoms like…

A

-Cognitive effects
-Anger
-Delusions
-Increased irritability
-Dysphoria
-Hostility

174
Q

Stage 3 of episode development is the progression of mania to a psychotic state; this includes symptoms like…

A

-Terror
-Hallucinations
-Frenzied activity
-Panic
-Bizzare behavior

175
Q

Symptoms of bipolar depression are not secondary to…

A

-Substance use
-General medical condition

176
Q

What are three examples of “step” based pharmacology for bipolar depression?

A

-Texas Medication Algorithm Project (TMAP)
-Systematic Treatment Enhance Program for Bipolar Disorder (STEP-BD)
-American Psychiatric Association (APA) Guidelines

177
Q

Acute stabilization for someone in a manic state will relieve the most ____ symptoms and resolve the episode

A

Severe

178
Q

The continuation phase of treatment lasts for ___-___ months after the end of the episode; this prevents relapse/cycling

A

2-6

179
Q

During the continuation phase of treatment, ___ ___ are adjusted and antipsychotics/benzodiazepines are tapered off

A

Mood stabilizers

180
Q

In the maintenance phase of bipolar disorder treatment, what two types of drugs are used?

A

-Mood stabilizers
-Antidepressants and antipsychotics

181
Q

What are some examples of mood stabilizers that might be used during the maintenance phase of bipolar treatment?

A

-Lithium (Lithobid, Eskalith)
-Carbamezapine (Tegretol, Tegretol-XR)
-Oxcarbazepine (Trileptal)
-Valproic Acid (Depakote, Depakote-ER)
-Lamotrigine

182
Q

More research is needed to make any definitive recommendations regarding the use of ____ and ____ in the maintenance phase of bipolar treatment

A

Antidepressants and antipsychotics

183
Q

____ is effective for manic phase and for long-term maintenance of bipolar

A

Lithium

184
Q

Lithium stabilized mood without causing ____

A

Sedation

185
Q

The effect of Lithium starts within days, but the full effect is seen within ___-___ weeks (the exact mechanism of Lithium is unknown)

A

2-4

186
Q

Lithium is not effective for rapid-cycling, but can decrease ____ of manic or depressive episodes

A

Frequency

187
Q

Lithium may be given with an ____ or ____ during a depressive episode

A

SSRI or bupropion

188
Q

Lithium is available in what dosage forms?

A

-Regular release
-Controlled release
-Syrup

189
Q

If someone is on Lithium, they should maintain proper ____ and ____ intake

A

Fluid, sodium

190
Q

Side effects of lithium include…

A

-Nausea
-Diarrhea
-Weight gain
-Polyuria
-Tremor
-Hypothyroidism

191
Q

What can cause an increase lithium level in the body if someone is taking lithium?

A

-Dehydration
-ACE inhibitors (Captopril, enalapril)
-Metronidazole
-NSAIDS
-Thiazide diuretics, phenothiazines, haloperidol, fluoxetine

192
Q

What can cause decreased lithium levels in the body if someone is taking lithium?

A

-Calcium channel blockers
-Theophylline (increases lithium excretion)

193
Q

What can cause increased neurotoxicity in someone taking lithium?

A

-Antipsychotics
-SSRI’s
-Haloperidol (Haldol)
-Neuroleptic Malignant Syndrome

194
Q

Mild/early symptoms of lithium toxicity develop gradually over several _____

A

Days

195
Q

Symptoms of mild lithium toxicity include…

A

-Ataxia
-Coarse tremor
-Confusion
-Diarrhea
-Drowsiness
-Muscle twitches
-Slurred speech

196
Q

Treatment for lithium toxicity:

A

-Hold doses
-Assessment of signs and symptoms
-Obtain lithium level
-Check vital signs
-Patient education

197
Q

Moderate/severe lithium toxicity (>2mEq/L) has either a ___ or ___ onset

A

Gradual or sudden

198
Q

Signs and symptoms of moderate/severe lithium toxicity include…

A

-Muscle tremor
-Hyperreflexia
-Pulse irregularities
-Hyper/hypotension
-EKG changes
-Visual/tactile hallucinations
-Oliguria/anuria
-Seizures
-Coma
-Death

199
Q

Treatment for moderative/severe lithium toxicity:

A

-Hold ALL doses
-Assessment of signs and symptoms of toxicity
-Obtain lithium level
-Check vital signs and consciousness
-Protect airway, O2
-BUN, SCr, urinalysis, CBC with diff
-ECG
-Hydration
-Gastric lavage, emetic
-Hemodialysis is the most reliable method

200
Q

Lithium is the ____ for drug therapy of bipolar due to 40 years of experience

A

Standard

201
Q

Lithium is the standard treatment for ___ ___ and ____

A

Euphoric mania and hypomania

202
Q

Lithium is effective for ____ and ____ therapy

A

Maintenance and prophylactic

203
Q

Lithium may provide more protection for patients with ____ during their episodes versus valproic acid

A

Suicidality

204
Q

Lithium can be used alone or in combination, has a variety of dosage forms, and is _____

A

Inexpensive

205
Q

If someone is on lithium, what types of laboratory evaluation should they receive?

A

-Renal
-Thyroid
-Cardiac
-CBC/diff
-Electrolytes

206
Q

One downside of lithium is that it has a ____ onset of effect

A

Slow

207
Q

Lithium has a ____ therapeutic index (acute: 0.8-1.2 mEq/L); maintenance: 0.6-1.0 mEq/L)

A

Narrow

208
Q

Lithium has many side-effects, which leads to ____

A

Noncompliance

209
Q

Carbamazepine (Tegretol, Tegretol-XR) is an _____ drug that may be used to treat acute mania or for prophylactic therapy

A

Anticonvulsant

210
Q

Carbamazepine (Tegretol) works well for stabilizing ____-____ patients

A

Rapid-cycling

211
Q

The max daily dose of Carbamazepine (Tegretol) is ____ mg/day

A

1200

212
Q

Therapeutic range of Carbamazepine (Tegretol) is between ___-___ micrograms/mL

A

4-12

213
Q

At concentrations of Carbamazepine over 8 micrograms/mL, patients may experience…

A

-Nausea
-Vomiting
-Lethargy
-Dizziness
-Drowsiness
-Headache
-Blurred vision
-Diplopia
-Ataxia

214
Q

Toxic effects of Carbamazepine (Tegretol) are typically seen when dosing changes are made ____

A

Abruptly

215
Q

Side effects of Carbamazepine:

A

-Blood dyscrasias (thrombocytopenia, leukopenia, rare aplastic anemia)
-Skin reactions: Steven-Johnson Syndrome
-Hyponatremia
-Cognitive effects (sedation, ataxia, dizziness)
-Neuromuscular effects

216
Q

What drugs increase Carbamazepine levels?

A

-Calcium channel blockers
-Cimetidine
-Erythromycin
-Valproate

217
Q

What drug decreases carbamazepine levels?

A

-Phenobarbital

218
Q

Carbamazepine causes decreased drug effects/levels of…

A

-Hormonal contraception
-Theophylline
-Warfarin

219
Q

Carbamazepine was approved for the management of ____ and paroxysmal ____ ____

A

Epilepsy; pain disorders

220
Q

A benefit of Carbamazepine is that is has a more ____ onset than Lithium

A

Rapid

221
Q

Generally, Carbamazepine is well-tolerated and may be more effective than Lithium for “___ ___” and “___ ___”

A

Mixed mania; rapid cyclers

222
Q

Carbamazepine is ____ and generally available

A

Inexpensive

223
Q

What are some disadvantages of Carbamazepine (Tegretol):

A

-Stimulates own oxidative metabolism
-Drug interactions
-Lab evaluation: CBC-differential; liver and kidney function

224
Q

Oxcarbazepine (Trileptal) has a similar mechanism of action to ____

A

Carbamazepine

225
Q

What are the indication for Oxcarbazepine (Trileptal)?

A

-Monotherapy or adjunctive for partial seizures in adults
-Adjunctive therapy of partial seizures for children

226
Q

Unlabeled uses of Oxcarbazepine (Trileptal) include…

A

-Acute mania
-Atypical panic disorder

227
Q

Side effects of Oxcarbazepine (Trileptal):

A

-Dose-dependent: headache, drowsiness, dizziness, ataxia, tiredness, nausea
-Idiopathic: hyponatremia, rash, weight gain

228
Q

Laboratory monitoring is ___ ___ for someone on Oxcarbazepine (Trileptal)

A

Not required

229
Q

There is an interaction between Oxcarbazepine and hormonal ____

A

Contraception

230
Q

Valproic acid (Divalproex-Depakote) is another anticonvulsant approved by the FDA in 1995 for use in ___ and ___ ____ states

A

Mania and mixed bipolar

231
Q

Valproic acid is useful in ___-___ bipolar patients

A

Rapid-cycling

232
Q

The max dose of valproic acid is ____ mg/kg/day

A

60

233
Q

The therapeutic range of Valproic acid is between ____ and ____ micrograms/mL

A

50-150

234
Q

Valproic acid toxicity is better tolerated than lithium, but more ____

A

Sedating

235
Q

At levels over 75 micrograms/mL of Valproic acid, someone might experience…

A

-Ataxia
-Sedation
-Lethargy
-Fatigue (decreased with continued usage)

236
Q

At levels over 100 micrograms/mL of Valproic acid, someone might experience…

A

-Tremor
-Trouble concentrating

237
Q

At levels over 175 micrograms/mL of Valproic acid, someone might experience…

A

-Stupor
-Coma

238
Q

Valproic acid may also cause more ___ ___ and ___ ___ than other anticonvulsants

A

Weight gain; hair loss

239
Q

Valproic acid cause cause ___ ___ Syndrome

A

Polycystic Ovary

240
Q

Valproic acid can rarely cause ____, more commonly in children

A

Hepatotoxicity

241
Q

The therapeutic range of Valproic acid is between ___-___ mg/day

A

750-3000

242
Q

Valproic acid may be administered as an oral ___ dose for inpatient treatment

A

Loading

243
Q

____ increases Valproic acid levels

A

Fluoxetine

244
Q

____ and ____ taken with Valproic acid increase bleeding time

A

Aspirin and Warfarin

245
Q

Valproic acid increases levels of ____ in the blood

A

Phenytoin

246
Q

____ is a monotherapy for generalized seizures in adults and children

A

Lamotrigine (Lamictal)

247
Q

Lamotrigine (Lamictal) can be used as adjunct therapy to ____ seizures (refractory)

A

Partial

248
Q

Lamotrigine (Lamictal) inhibits the release of ____, which is an excitatory amino acid

A

Glutamate

249
Q

Labeled use of Lamotrigine (Lamictal) is for…

A

-Maintenance mood stabilizer in bipolar I depression

250
Q

Unlabeled use of Lamotrigine (Lamictal) is for…

A

-Mood stabilizer in rapid cycling bipolar II

251
Q

Dosage of Lamotrigine (Lamictal) is reduced by 50% when taken with ___ ____ because it will cause a rash

A

Valproic acid

252
Q

Lamotrigine (Lamictal) has no interaction with hormonal ____

A

Contraception

253
Q

Lamotrigine (Lamictal) is a pregnancy category ____ drug, but may be updated to category C

A

B

254
Q

Adverse effects of Lamotrigine (Lamictal):

A

-Dizziness
-Headache
-Diplopia
-Ataxia
-Nausea
-Blurred vision
-Somnolence
-Skin rash

255
Q

Topiramate (Topamax) is approved for partial and complex ____, but not for bipolar disorder

A

Seizures

256
Q

There have been no systematic studies to establish ___ or ____ of Topiramate (Topamax) for mood disorders

A

Safety, efficacy

257
Q

Topiramate (Topamax) may be useful for “hard-to-treat” or “resistant” patients with comorbid ____ ___ and ___ ___ disorders

A

Substance abuse; impulse control

258
Q

Topiramate (Topamax) is usually dosed in addition to other ____ ____

A

Mood stabilizers

259
Q

The dosage titration rate of Topiramate (Topamax) is limited by ____ ____

A

Cognitive dulling

260
Q

Topiramate (Topamax) may be helpful in minimizing ____ ____ from other medications

A

Weight gain

261
Q

Topiramate (Topamax) has a possible interaction with hormonal _____

A

Contraception

262
Q

What are some adverse effects of Topiramate (Topomax)?

A

-Somnolence
-Dizziness/vision problems
-Unsteadiness
-Nervousness
-Nausea
-Hot flashes (increases body temp; caution against use in children)

263
Q

Gabapentin (Neurontin) is effective for the treatment of…

A

-Complex partial seizures
-Generalized seizures
-Neuropathic pain

264
Q

Gabapentin (Neurontin) is not effective for the treatment of ____ disorders (only agent to date to test worse than placebo)

A

Bipolar

265
Q

2/3 patients are unresponsive to ____ monotherapy

A

Lithium

266
Q

What are four possible drug regimens for refractory patients?

A

-Lithium + anticonvulsant
-2 anticonvulsants
-Lithium + 2 anticonvulsants
-Levothyroxine for rapid cyclers

267
Q

_____ can be used for acute management of bipolar disorder

A

Benzodiazepines

268
Q

Antidepressants are less likely to produce robust, sustained responses in ____ disorders

A

Bipolar

269
Q

“_____ _____” are treatment-emergent events that are not uncommon; they include mania/hypomania, rapid cycling states, and treatment resistance

A

Antidepressant misadventures

270
Q

When would antidepressants be indicated for bipolar depression?

A

-Patients who cannot wait 4-6 week delay before a response to mood stabilizer
-Patients who have a history of response to previous treatment with antidepressants
-Patients who have not responded to mood stabilizers or psychotherapy in the past

271
Q

We should try to limit antidepressant use to the management of ____ episodes of bipolar

A

Acute

272
Q

Antidepressants may accelerate the course of bipolar disorder and induce ____ ____

A

Rapid cycling

273
Q

Antidepressants mainly induce a switch to ____, especially with TCAs

A

Mania

274
Q

If antidepressants are used for bipolar, there should be simultaneous use of a ___ ___

A

Mood stabilizer

275
Q

Patients experiencing a depressive episode should stay on antidepressants for ___-___ months, and then slowly taper on a patient-by-patient basis

A

6-12

276
Q

Some patients may require a maintenance antidepressant adjunctively with their maintenance ____ ____

A

Mood stabilizer

277
Q

If someone needs to be on an antidepressant for bipolar, ____ might be a good choice since it may be less likely than TCAs to induce a switch (SSRIs, venlafaxine, nefazodone, and mirtazapine would also be options)

A

Bupropion

278
Q

What are three mood stabilizer options for those with BPD?

A

-Lamotrigine
-Lithium
-Carbamazepine (?)

279
Q

What drugs are given to patients during a state of mania or hypomania?

A

-Benzodiazepines
-Antipsychotics (Haldol)
-Atypical antipsychotics

280
Q

What are the indications of benzodiazepines for BPD?

A

-May have faster onset for non-psychotic agitation

281
Q

What are two examples of Benzodiazepines that may be used for the treatment of BPD?

A

-Lorazepine (Ativan)
-Clonazepam (Klonapin)

282
Q

Lorazepam (Ativan) can be given by mouth or IM, and should be tapered when _____ stabilizes, about 1-2 weeks

A

Agitation

283
Q

Clonazepam (Klonopin) is the agent of choice (long-acting) in patients with prior history or susceptible to ____ abuse

A

Substance

284
Q

What are the indications of atypical antipsychotics for patients with BPD?

A

-Acute treatment of mixed or psychotic mania
-Maintenance treatment and prophylaxis

285
Q

What is the proposed mechanism of antipsychotics for the treatment of BPD?

A

-Enhancing serotonin and norepinephrine activities reduce symptoms of mood and anxiety
-Antagonize serotonin and alpha-2-adrenergic receptors to varying degrees
-May have an earlier onset of therapeutic effect versus “traditional mood stabilizers”

286
Q

Indication of Aripiprazole (Abilify) for BPD:

A

-Acute mania and maintenance

287
Q

Indication of Olanzapine (Zyprexa) for BPD:

A

-Acute mania and maintenance

288
Q

Indication of Olanzapine/Fluoxetine (Symbyax) for BPD:

A

-Acute mania and maintenance

289
Q

Indication of Quetiapine (Seroquel) for BPD:

A

-Acute mania

290
Q

Risperidone (Risperdal) is FDA approved in ___ and ___

A

Children and adolescents

291
Q

All patients receiving an “atypical antipsychotic” must receive monitoring for the potential development of…

A

-Weight gain
-Obesity
-T2D
-Metabolic syndrome

292
Q

There is a high rate of relapse within ___ months following remission of an acute episode; we should use an antipsychotic to control persistent psychosis or as prophylaxis against recurrence

A

6

293
Q

What are some alternative pharmacotherapies for bipolar disorders?

A

-Thyroid hormone (T3 and/or T4)
-Electroconvulsive therapy
-Pramipexole (Mirapex)
-Omega-3 fatty acids

294
Q

____ hormone would be adjuvant therapy and may be more useful in “rapid cyclers”

A

Thyroid

295
Q

Electroconvulsive therapy may be preferred when a patient’s behavior is extremely ___ ____ and a rapid response is needed

A

Life threatening

296
Q

Pramipexole (Mirapex) should be used in cation with people who have history of impulse control disorders and ____

A

Addictions

297
Q

Mood stabilizers are not recommended to mothers while ____ because they can transfer to the child

A

Lactating

298
Q

What agents should be avoided while a mother is lactating?

A

-Valproic acid
-Lithium

299
Q

Lithium during pregnancy can cause ____ ____

A

Epstein’s anomaly

300
Q

Carbamazepine during pregnancy can cause…

A

-Neural tube defects
-Craniofacial defects

301
Q

Valproic acid during pregnancy can cause…

A

-Neural tube defects

302
Q

Treatment of bipolar during the postpartum period includes…

A

-Prophylactic mood stabilizer in women with BPD during the postpartum period
-Resume mood stabilizer treatment a few days after delivery

303
Q

Patients should discontinue mood stabilizers during the ____ trimester if possible

A

1st

304
Q

If mood stabilizers much be given during pregnancy, ____ _____ counseling should be given and fetal monitoring at 16-18 weeks gestation should be done using high resolution ultrasound

A

Reproductive risk

305
Q

If a pregnant mother is on mood stabilizers, serum and fluid ____ levels should be checked and a fetal echocardiography should be done

A

a-fetoprotein

306
Q

Patients should discontinue mood stabilizers a few days before ____ to minimize toxic effects on the infant

A

Delivery

307
Q

What are steps for implementing a plan to achieve remission in those with BPD?

A

-Assure the patient can pay for medication
-Make information available to patient
-Encourage patient to self-monitor
-Individualization of medication, incorporating patient preferences
-Assume patient can recognize emergence of recurrent symptoms and follow up with treating clinician
-Consider concomitant disorders
-Alert patients to side effects
-Verify current and previous medical history

Advanced Pharmacology (10 decks)

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