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Block 8 Week 1 > Antidepressants and Mood Stabilizers-Craviso > Flashcards

Antidepressants and Mood Stabilizers-Craviso Flashcards

1
Q

Currently available drugs are based on the (blank) hypothesis of depression

A

monoamine

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2
Q

All the antidepressants cause immediate effects on synaptic (blank) levels

A

monoamine

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3
Q

How long does it take for antidepressants to kick in? Why?

A

one or more weeks

-due to slow increase in expression of BDNF that promotes synaptogenesis

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4
Q

Which antidepressant class is superior?

A

there isnt one

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5
Q

At least (blank) percent of all depressed patient are refractory to multiple different antidepressants at adequate doses

A

20%

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6
Q

What are the four major classes of antidepressant drugs?

What is the first line drug?

A
  1. SSRI
  2. SNRI
  3. MAOis
  4. New drugs

SSRI and SNRIs are first line drugs

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7
Q

What do SSRIs work?

A

block 5-HT reuptake

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8
Q

What are serotonin-norepinephrine reuptake inhibitors?

A
  • newer “selective” inhibitors - block NE and 5-HT reuptake

- older, less selective inhibitors-tricyclics (TCA) that exert antagonist effects on a variety of receptors

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9
Q

How do the newer antidepressants work?

A
  • inhibit reuptake of dopamine

- agonist/antagonist activities at certain types of 5-HT and NE receptors

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10
Q

How do Monamine oxidase inhibitors work?

A

inhibit the metabolism of NE and 5-HT

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11
Q

What AA does serotonin come from?

What AA does NE come from?

A

tryptophan

tyrosine

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12
Q

What are the five famous SSRIs (first line drugs)?

A
  • Fluoxetine (prozac)
  • Sertraline (Zoloft)
  • Paroxetine (Paxil)
  • Citalopram (Celexa)
  • Escitalopram (Lexapro)
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13
Q

How are SSRIs metabolized?

A

in the liver

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14
Q

What are SSRIs potent inhibitors of?

A

several cytochrom P-450 enzymes (CYP2D6)

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15
Q

Fluoxetine and Paroxetine are (low/high potential) cytochrome P450 inhibitors?

A

High potential

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16
Q

Citalopram (celexa) and Escitalopram (lexapro) are (low/high potential) cytochrome P450 inhibitors?

A

low potential

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17
Q

What are the adverse side effects of SSRIs?

A
  • Signif sexual dysfunction
  • Gi disturbance
  • Insomnia, restlessness
  • anorexia and weight loss (early treatment)
  • Weight gain (long term)
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18
Q

What SSRI can give you QT prolongation?

A

Citalopram

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19
Q

Use of (blank) during pregnancy linked to an increased risk for cardiovascular

A

paroxetine

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20
Q

How can you get 5-HT syndrome when giving SSRIs?

A

You give them with MAO inhibitors or other drugs that enhance 5-HT neurotransmission

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21
Q

WHy dont you want to give antidepressants to children, adolescents and young adults really?

A

because it can worsen their depression (suicide)

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22
Q

What is the only SSRI approved for use in children and adolescents?

A

Fluoxetine

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23
Q

What is an SSRI approved for use in adolescents?

A

escitalopram

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24
Q

What can you use SSRIs for other than treatment for depression?

A
  • anxiety
  • seasonal affective disorder
  • bulimia nervosa
  • migraine prophylactic
  • PMS and PMDD, hot flashes
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25
Q

What SSRI do you give for seasonal affective disorder?

A

paroxetine

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26
Q

What SSRI do you give for bulimia nervosa?

A

fluoxetine

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27
Q

What SSRI do you give for PMS and PMDD (most); hot flashes?

A

paroxetine

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28
Q

What are the 2 newer “selective” inhibitors (SNRIs)?

A

Venlafaxine (effexor, effexor ER)

Duloxetine (Cymbalta)

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29
Q

What does Venlafaxine do?

A

block reuptake of both NE and 5-HT

-weakly inhibits DM uptake

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30
Q

What are the adverse SEs of Venlafaxine (effexor)?

A

resemble those of SSRIs (sexual dysfunction, GI, restlessness, insomnia)

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31
Q

What are some additional uses of Venlafaxine?

A

anxiety disorders

-treatment of neuropathic pain

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32
Q

What are the adverse side effects of Duloxetine (cymbalta)?

A

contraindicated for those with chronic liver disease or hepatic insufficiency

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33
Q

What are some additional uses of Duloxetine (cymbalta)?

A
  • management of fibriomyalgia
  • management of diabetic peripheral neuropathy
  • long term treatmetn of generalized anxiety disorder (GAD)
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34
Q

What do tricyclic antidepressants do ?

A

THey are old SNRIs and block the reuptake of both NE and 5-HT to varying degrees

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35
Q

What are the three important tricyclic antidepressants?

A

nortriptyline (aventyl, pamelor)
impiramine (tofranil)
amitriptyline (elavil)

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36
Q

What does nortriptyline (aventyl, pamelor) block mostly?

A

Norepinephrine (mostly) and seritonin (a little)

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37
Q

What does imipramine (tofranil) and amitryiptyline (Elavil) block mostly?

A

seritonin (mostly) and NE (a little)

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38
Q

Why arent tricyclic antidepressants first line drugs anymore?

A
  • can be fatal in overdose
  • are cardiotoxic
  • lower seizure threshold
  • have signif antagonist activity at several types of neurotransmitter receptors
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39
Q

WHo do you give tricyclic antidepressants to?

A

patients who do not respond or tolerate more widely-prescribed antidepressants.

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40
Q

What can amitriptyline be used for other than depression?

A

migraine prophylactic

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41
Q

Tricyclic antidepressants (TCAs) have more effects than blocking 5-HT and NE reuptake. What are the three other receptors that TCAs block?

A

mACh, alpha 1, histamine 1

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42
Q

What TCA blocks the mACh, alpha 1 and histamine 1 receptors the most?

A

amitriptyline (elavil)

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43
Q

What TCA blocks the mACh, alpha 1 and histamine 1 receptors the least?

A

nortriptyline (aventyl, pamelor)

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44
Q

What will blocking of mACh receptors cause?

A
  • sedation
  • cognitive impairment
  • confusion
  • delirium
  • blurred vision
  • dry mouth
  • tachycardia
  • urinary retention
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45
Q

What will blocking of alpha 1 receptors cause?

A

orthostatic hypotension

sedation

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46
Q

What will blocking of histamine 1 receptors cause?

A

sedation

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47
Q

At therapeutic doses all TCAs can cause what SEs?

A

lowering of seizure threshold
sexual dysfunction
weight gain

48
Q

So what is the worst TCA?

A

amitriptyline (elavil) (it can block too many things)

49
Q

At toxic doses what can TCAs cause?

A

cardiotoxicity-(cardiac conduction delays Q-T prolongation, ventricular block, arrhythmias (ventricular tachycardia)

50
Q

The therapeutic index for TCAs is (blank) and some patients may develop cardiotoxicity at therapeutic doses

A

low

51
Q

Acute overdose of TCAs is often life-threatening due to …..?

A
  • hyperpyrexia
  • hypertension
  • tachycardia
  • arrhythmias
  • severe anticholinergic effects
  • convulsions
52
Q

What drugs can cause drug interactions with TCAs?

A
  • MAO inhibitors
  • anticholinergics
  • antihistamines
  • CNS depressants
53
Q

If you take a TCA with an MAOI at the same time, what can happen?

A

severe hypertension, rick of 5-HT syndrome

54
Q

If you take a TCA with an anticholinergic or antihistamine, what can happen?

A

an additive effect due to blockade of mACH and H1 receptors by TCA

55
Q

If you take a TCA with a CNS depressant, what can happen?

A

sedation

56
Q

What is a well known dopamine reuptake inhibitor?

A

bupropion (wellbutrin)

57
Q

Dopamine reuptake inhibitors such as bupropion can possibly block the reuptake of (blank and blank)

A

NE

5-HT

58
Q

What are the adverse SEs of bupriopion (wellbutrin)?

A
  • restlessness, insomnia, anxiety
  • risk of seizure activity (dose-related)
  • can precipitate psychotic episodes
59
Q

What patients is buproprian (wellbutrin) contraindicated in?

A

patients with a history of seizures and eating disorders

60
Q

How come bupropion (wellbutrin) can precipitate psychotic episodes?

A

excessive dopamine in susceptible individuals

61
Q

Does bupropion (wellbutrin) have more or less sexual side effects compared to other antidepressants?

A

less

62
Q

(blank) can be used as an aid in smoking cessation.

A

bupropion (sustained release formulation -Zyban)

63
Q

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

A

antagonist of central presynaptic alpha-2 adrenergic autoreceptors (receptors that mediate negative feedback for NE and 5-HT release i.e increase NE and 5-HT release)
-blockades 5HT2 an 5HT3 receptors

64
Q

What are the adverse side effects of Mirtazapine (remeron)?

A
  • sedation, somnolence
  • dizziness
  • stimulates appetite, signif weight gain
65
Q

Does mirtazapine (remeron) have a lot of sexual side effects?

A

no

66
Q

How does trazodone work?

A

blocks 5 ht reuptake

-antagonist at 5HT2 receptors and partial agonist at 5HT1 receptors

67
Q

What are some adverse SEs associated with Trazodone (Desyrel)?

A
  • signif drowsiness and dizziness
  • GI upset (nausea and vomiting)
  • orthostatic hypotension
  • protracted erection (priapism)
68
Q

What is the mechanism of action of Vilazodone (Vibryd)?

A

a SSRI and a partia agonist at 5-HT1a receptors

69
Q

What are the adverse effects of Vilazodone (vibryd)?

A

insomnia

GI disturbances

70
Q

Does Vilazodone (vibryd) cause sexual side effect and weight gain?

A

no

71
Q

What are the three drugs with agonist/antagonist activities at certain types of 5-HT and NE receptors?

A

Vilazodone (Vibryd)
Trazodone (Desyrel)
Mirtazapine (Remeron)

72
Q

What is MAO?

A

enzyme in nerve terminals that converts the monoamine neurotransmitters NE, 5-HT, and dopamine into inactive products

73
Q

THere are 2 types of MAO, what does MAO-A metabolize?

A

NE and 5-HT

74
Q

THere are 2 types of MOA, what does MAO-B metabolize?

A

dopamine

75
Q

What is the last choice antidepressant? Why?

A

MAOI

risk of hypertensive crisis in response to ingestion of certain foods (tyramine) and drugs during MAOI use.

76
Q

What can you use MAOIs to treat other than depression?

A

Parkinson’s disease

77
Q

What happens if you are on an MAOI and then you eat tyramine?

A

tyramine will displace norepinephrine and you will get a hypertensive crisis

78
Q

What is a MAOI that is a reversible inhibitor?

A

Selegiline (Eldepryl)

79
Q

What is a MAOI that is an irreversible inhibitor?

A

Phenelzine (Nardil)

80
Q

What is Ensam?

A

it is selegiline that is available transdermally

81
Q

Why would you want to give selegiline transdermally (Ensam)?

A

so it can bypass the gut and inhibit central MAO enzymes wihile reducing the chance of hypertensive reactions caused by tyramine

82
Q

What are the adverse side effects of phenelzine (nardil)?

A
  • Anorgasmia or sexual impotence
  • CNS stimulation (restlessness, insomnia)
  • sleep disturbances (inhibit REM sleep)
  • weight gain
  • Orthostatic hypotension
83
Q

You get drug interactions with MAOI when you take them with

A
  • indirect acting sympathomimetics and tyramine-containing food (hypertensive crisis)
  • SSRIs and 5-HT receptor agonists (5-HT syndrome)
84
Q

If you see drug names with 2 Es and a ZINE or a LINE at the end what kind of drugs are they?

A

MAOIs

85
Q

What characterizes a manic episode?

A
  • exaggerated optimism and self-confidence
  • decreased sleep w/out experiencing fatigue
  • grandiose delusions, inflated sense of self-importance
  • excessive irritability; aggressive behavior
  • racing speech, flight of ideas
  • easily distracted
  • impulsiveness, poor judgement
  • reckless behavior
86
Q

Depressive and manic episodes last for several weeks to several months, often with (blank) in between swings

A

normal mood

87
Q

What is considered rapid cycling in bipolar disorder?

A

more than 4 full cycles per year (rare)

88
Q

What is the first line drug for acute mania and long-term maintenance therapy to avert manic and depressive episodes in patients with bipolar disorder?

A

lithium

89
Q

What are the 2 types of lithium you can give?

A 
lithium carbonate (Eskalith-CR)
lithium citrate (Cibalith-S)
90
Q

Why dont you want to give antidepressants to a bipolar patient?

A

can trigger mood swings

91
Q

What isn’t effective for rapid cyclers?

A

lithium

92
Q

Sometimes you will combine lithium with (blank) in bipolar patients initially during depressive episodes but use caution

A

SSRI

93
Q

The mechanism behind lithium is unknown but it involves long-term (blank) changes

A

neuroplastic

94
Q

What are the immediate effects of lithium?

A
  • inhibition of recycling of inositol substrates

- altering the function of G-proteins associated with Beta-adrenergic and M1 ACh receptors

95
Q

How does lithium distribute in the body?

A

into total body water

96
Q

When do you get peak plasma levels of lithium?

A

1-2 hours standard prep

4 hours with slow release formula

97
Q

How does lithium get eliminated and what is its half-life?

A

kidney

20-24 hours

98
Q

Renal clearance is proportional to (blank) concentration

A

plasma

99
Q

What all can increase lithium levels?

A

renal problems, CHF, dehydration, advanced age

100
Q

When you take lithium, you willl retain lithium at the expense of what ion?

A

sodium

101
Q

Lithium clearance is decreased by what 3 drugs?

A

NSAIDs
loop and thiazide diuretics
ACE inhibitors

102
Q

Lithium clearance is increased with what four drugs?

A

caffeine
osmotic diuretic
acetazolamide
theophylline

103
Q

What do you use acetazolamide for?

A

Edema-> its a diuretic

104
Q

What is the therapeutic plasma level of lithium?

A

0.5-1.5 mEq/l

105
Q

What are the adverse SEs of lithium at therapeutic levels?

A
  • drowsiness, slowed mentation and forgetfullness
  • GI disturbances (nausea, vomiting, diarrhea)
  • polyuria and thirst (decreased response of kidney to ADH)
  • weight gain
  • mild tremor (principally in the fingers)
106
Q

What are the adverse SEs of lithium with long-term use?

A
  • degenerative changes in the kidney (interstitial nephritis)
  • depression of thyroid function (goiter) due to interference with iodine use in the thyroid
107
Q

When shouldnt you take lithium and why?

A

pregnancy and breast feeding

-> can cause Ebstein’s anomaly

108
Q

Lithium has a (blank) therapeutic index so serum levels must be carefully monitored

A

low (always monitor for conditions that my decrease clearance or volume of distribution)

109
Q

Above 2.5 mEq/ lithium produces…..(4)?

A
  • ataxia
  • gross tremor
  • cardiac arrhythmias
  • coma and convulsions (can cause death)
110
Q

When can you see toxicity of lithium in the blood?

A

you can see toxicity at any blood level

111
Q

What is valproic acid (depakote, depakote ER)?

A

an antiepileptic drug (AED) and used to treat mania and mixed states

112
Q

Whats the downside of treating bipolar disorder with valproic acid (depakote)?

A

shows good efficacy relative to lithium in the acute and long-term BUT can be more sedating than lithium

113
Q

What is carbamazepine (tegretol, tegretol XR, equetro)?

A

antiepileptic drug (AED) used to treat mania and mixed states

114
Q

What are the 6 atypical antipsychotics?

A
  • quetiapine (seroquel)
  • aripiprazole (abilify)
  • olanzapine (zyprexa)
  • lurasidone (latuda)
  • asenapine (saphris)
  • risperidone (risperdal)
115
Q

What do you give lurasidone (latuda) for?

A

bipolar depression

116
Q

What are the 2 famous benzodiazepines?

A

Lorazepam (ativan)

Clonazepam (klonopin)

117
Q

What is a new AED used also for bipolar depression?

A

Lamotrigine (lamictal)

Block 8 Week 1 (13 decks)

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