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Pharmacology Test #6 > Mood Disorder Pharmacology > Flashcards

Mood Disorder Pharmacology Flashcards

1
Q

Criteria for major depressive disorders

A
  1. Depressed mood for 2+ weeks
  2. Anhedonia
  3. Anxiety
  4. Disrupted sleep/appetite
  5. Cognitive deficits
  6. Loss of self-worth
  7. Suicidal thoughts
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2
Q

Co-morbid medical/psychiatric conditions with major depressive disorders

A

CAD, diabetes, stroke, chronic pain, drug abuse

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3
Q

Monoamine hypothesis

A

MDD caused by a deficiency in cortical/limbic 5HT, NE, DA

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4
Q

Two theories of depression that are non-mutually exclusive

A

the monoamine hypothesis and the neurotrophic hypothesis

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5
Q

Evidence for the monoamine hypothesis

A
  1. Reserprine (monoamine depleter) causes depression
  2. Dietary changes: patients treated with AD relapse when tryptophan is withdrawn from diet
  3. Genetics: SNPs in SERT associated with MDD
  4. 5HT, NE receptors are decreased in MDD patients
  5. 5HT/NE/DA agents work
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6
Q

Neurotrophic hypothesis

A

MDD is caused by loss of neurotrophic support and ADs restore neurogenesis and lost synaptic connectivity

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7
Q

Brain-derived neurotropic factor (BDNF) and neurons in a normal state

A

cell receives input from monoamine and BDNF stimulation, which supports neurotrophy and synaptic connectivity

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8
Q

BDNF and neurons in a depressed state

A

in part due to interference via glucocorticoids, BDNF is reduced and results in hypotrophy and loss of connectivity

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9
Q

BDNF and neurons in a treated state

A

monoamines result in increased CREB expression and results in resumption of normal BDNF secretion, re-gained connectivity

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10
Q

BDNF is critical for

A

neurotrophic support and required for the action of ADs

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11
Q

Evidence for the neurotrophic hypothesis:

A
  1. BDNF changes in MDD: stress/pain reduces BDNF, causing structural changes in hippocampus similar to that seen in MDD
  2. BDNF has AD properties: direct infusion of BDNF in rodent has AD effect
  3. ADs cause increased BDNF/neurogenesis
  4. Human MDD and BDNF: MDD associated with drop in BDNF
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12
Q

Why do antidepressants exhibit a delayed onset of several weeks compared to when their biochemical effects are thought to occur?

A

Time for monoamines to changes synthesis of BDNF, time for restored synaptic connectivity, and time for changes to occur such as up-or down-resgulation in signal transduction machinery

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13
Q

Antidepressant drug classes:

A
  1. SSRIs
  2. SNRIs (Serotonin-NE Reuptake Inhibitors)
  3. 5-HT2 Antagonists
  4. Tetracyclic/Unicyclic antidepressants
  5. MAOIs
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14
Q

SSRIs

A
  1. Fluoxetine (Proxac)
  2. Paroxetine (Paxil)
  3. Fluvoxamine (Luvox)
  4. Sertraline (Zoloft)
  5. Citalopram (Celexa)
  6. Escitalopram (Lexapro)
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15
Q

Which SSRIs inhibit P450s?

A
  1. Fluoxetine (Proxac)
  2. Paroxetine (Paxil)
  3. Fluvoxamine (Luvox)
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16
Q

What are SSRIs selective for?

A

more selective for SERT over NET

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17
Q

First choice for treatment of MDD due to safety and efficacy considerations

A

SSRIs

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18
Q

SSRIs Indications

A

MDD; Anxiety disorders; Premenopausal Dysphoric disorder; Eating disorders (bulimia only)

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19
Q

GAD

A

generalized, free-floating anxiety/undue worry

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20
Q

OCD

A

chronic anxiety-provoking thoughts (obsessions) and temporary anxiolytic actions (compulsions) taken to alleviate the anxiogenic thoughts

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21
Q

PTSD

A

anxious thoughts, hypervigilance from a traumatic event

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22
Q

Adverse effects of SSRIs

A
  1. Sexual dysfunciton
  2. Weight gain/loss
  3. Serotonin syndrome
  4. Adolescent suicide
  5. Withdrawal sndrome
  6. Effects on newborns
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23
Q

SSRI withdrawal

A

dizziness, paresthesias

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24
Q

Effects on newborns when mothers are on SSRIs

A

persistent pulmonary HTN (serious, fatal sometimes); withdrawal signs in infants; congenital malformations

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25
Q

Newer SNRIs

A
  1. Duloxetine (Cymbalta)
  2. Venlafaxine (Effexor)
  3. Desvenlafaxine (Pristiq)
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26
Q

Two classes of SNRIs

A

the older TCAs and a newer group of pure re-uptake inhibitors that hit NET with high affinity

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27
Q

Tricyclic Antidepressants (TCA)

A
  1. Amitriptyline (many receptors hit)
  2. Nortriptyline (secondary amine)
  3. Imipramine (anticholinergic)
  4. Desipramine (metabolite of imipramine)
  5. Clomipramine
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28
Q

Clinical use of TCAs

A

Used only in refractory MDD (not responsive to SSRIs)

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29
Q

Indications of SNRIs

A

Refractory MDD; anxiety disorders; pain (diabetic neuropathy, fibromyalgia); enuresis (bed wetting); insomnia

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30
Q

Adverse effects of SNRIs (most apply to the TCAs)

A
  1. Cardiotoxicity
  2. Sexual dysfunction
  3. Weight loss
  4. Serotonin syndrome (TCA and MAOI co-admin)
  5. Suicidal thoughts
  6. Withdrawal syndrome
  7. Sedation
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31
Q

Cardiotoxicity from SNRIs

A

derives from the ability to block voltage gated sodium channels in the heart, plus the anticholinergic properties as well; high BP, ventricular arrhythmias

32
Q

5HT2 Antagonist

A

Trazodone

33
Q

Patients on trazodone should avoid

A

grapefruit juice as it blocks CYP3A4, the same CYP that metabolizes trazodone

34
Q

Bupropion

A

unicyclic antidepressant; DA and NE reuptake inhibitor; no 5HT systemo activity; nAchR antagonist activity

35
Q

Adverse effects of Buproprion

A

few sexual side effects, some insomnia, anorexia, agitation, seizures

36
Q

Use of Buproprion

A

AD, mood enhancer, smoking cessation

37
Q

Mirtazapine

A

tetracyclic antidepressant; mixed antagonist or inverse agonist activity at 5HT, alphaAR, histamine, mACh, DA, NET, DAT, and SERT; stimulates release of NE and 5HT yet blocks 5HT receptors

38
Q

Adverse effects of Mirtazapine

A

few sexual, sedative (histamine), low cardio risk

39
Q

Use of Mirtazapine

A

refractory MDD, other mood disorders

40
Q

Monoamine Oxidase Inhibitors

A
  1. Selegiline (MAO-b, irreversible)
  2. Tranylcypromine (non-selective, irreversible)
  3. Phenelzine (non-selective, irreversible)
41
Q

MAO Type A

A

found in monoamine-expressing neurins in the CNS

42
Q

MAO Type B

A

found in DA neurons and in cells that need to break down phylethylamine and other trace amines

43
Q

When would you use MAOIs

A

used in cases of refractory MDD

44
Q

Adverse effects of MAOIs

A

orthostatic hypotension, sexual dysfunction, and CNS stimulant-like properties

45
Q

TCA overdose

A

mainly a cardiovascular event, such as arrhythmia and BP changes, but also includes CNS activation, anticholinergic effects and seizures

46
Q

TCA overdose treatment

A

usually directed toward the cardiovascular symptoms

47
Q

MAOI overdose

A

characterized by a hyperadrenergic state, including psychosis, confusion, fever and seizures

48
Q

MAOI overdose treatment

A

cardiac monitoring, HCO3

49
Q

5HT syndrome

A

A poisoning due to overstimulation of 5HT receptors - not an idiosyncratic drug reaction; likely in central gray nuclei/medulla in brain stem, likely 5HT2A

50
Q

Severe side effects of 5HT syndrome

A

delirium, coma, hypertension, tachycardia, diaphoreses, clonus, hyperreflexia, tremor, akathisia (agitation, restlessness)

51
Q

How do you prevent serotonin syndrome?

A

stop other ADs 2-4 weeks prior to starting MAOI (fluoxetine in particular); stop MAOI at least 2 weeks prior to starting/switching to SSRI (or other 5HT agent)

52
Q

What is the Tyramine Effect

A

MAOI prevents tyramine breakdown in the gut; tyramine builds up in the serum and acts as a peripheral only catecholamine releasing agent; noradrenergic effects are enhanced

53
Q

What is a bad combination with non-selective MAOIs

A

Tyramine-rick foods (meat, cheese, dairy, many others)

54
Q

Result of the Tyramine Effect

A

malignant hypertension, stroke, MIs

55
Q

Prevention of the Tyramine Effect

A

low-tyramine diet, use MAO-B inhibitor, use reversible MAOIs, avoid other sympathomimetics (pseudoephedrine, phenylpropanolamine) combined with MAOIs

56
Q

Herbal Antidepressants

A

St. John’s Wort (Hypericum perforatum plant)

57
Q

MOA of St. John’s Wort

A

monoamine reuptake block though some uncertainty exists

58
Q

Defining feature of bipolar disorder

A

Mania

59
Q

Symptoms of mania

A

hyperactivity, impulsive, disinhibition, aggression, less sleep, psychosis, cognitive impairment

60
Q

Bipolar I

A

extreme manic episodes; depressive episodes; recurring; rapid cycling (>4 per year); more severe

61
Q

Bipolar II

A

hypomanic episodes; depressive episodes often dominant; some functionality during hypomania; less severe

62
Q

Drug classes for Bipolar Disorder

A

Lithium carbonate
Atypical antipsychotics
Antiepileptics
Benzodiazepines

63
Q

First-choice drug for bipolar

A

Lithium carbonate

64
Q

Atypical antipsychotics

A

Aripiprazole, olanzapine, paliperidone, quetiapine, risperidone, ziprasidone, (clozapine)

65
Q

Antiepileptics

A

Carbamazepine, valproate, (levetiracetam, primidone, zonisamide)

66
Q

MOA for lithium

A

largely unknown and highly speculative; may be inositol depletion which may alter signaling systems or change plasticity; may be from inhibition of GSK-3

67
Q

What must you monitor with lithium

A
  1. plasma lithium levels
  2. Diuretic usage
  3. Sodium in diet should be consistent
  4. Exercise
68
Q

Why must you follow diuretic usage with lithium

A

diuretics can reduce the clearance of lithium, which would require the dose of lithium to be lowered

69
Q

Hallmark feature of lithium side effects

A

tremor which can be treated with a beta blocker

70
Q

Side effects of lithium

A

tremor, low thyroid fxn, edema, arrhythmias

71
Q

Lithium overdose

A

cognitive disturbances, GI issues, ataxia, nystagmus, slurred speech, muscle spasms

72
Q

What has replaced lithium in chronic treatment of bipolar

A

anticonvulsants

73
Q

What are antipsychotics/benzodiazepines used for

A

severe mania

74
Q

1st line maintenance therapy for bipolar disorder

A

Lithium (plus benzo in severe); Lamotrigine; Risperidone

75
Q

2nd line maintenance therapy for bipolar disorder

A

aripiprazole, quetiapine, olanzapine; and valproate

76
Q

Other options for maintenance therapy for bipolar disorder

A

carbamazepine, combination therapy

Pharmacology Test #6 (12 decks)

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