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Therapeutics III > Watts Antidepressants > Flashcards

Watts Antidepressants Flashcards

1
Q

Types of depression

A

-Reactive (60%)
-Major depressive disorder (25%)
-Bipolar affective (15%)

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2
Q

Physiological symptoms of depression

A

-Decreased sleep
-Appetite changes
-Fatigue
-Psychomotor dysfunctions
-Menstrual irregularities
-Palpitations
-Constipation
-Headaches
-Nonspecific body aches

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3
Q

Psychological symptoms of depression

A

-Dysphoric mood
-Worthlessness
-Excessive guilt
-Loss of interest/pleasure in all or most activities

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4
Q

Cognitive symptoms of depression

A

-Decreased concentration
-suicidal ideation

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5
Q

What must be ruled out when diagnosing depression?

A

It is not caused by drugs, medical conditions, or bereavement

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6
Q

What drugs can cause drug-induced depression?

A

-Antihypertensive and Cardiovascular
-Sedative-hypnotics
-Anti-inflammatory and analgesics
-Steroids
-Anti-Parkinson
-Anti-neoplastic
-Neuroleptics

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7
Q

What is the biogenic amine hypothesis of depression?

A

-Reserpine causes depression by deleting NE and 5HT from vesicles
-Agents that increase 5HT and NE are effective for treating depression
-Genetic polymorphisms in SERT promoter
-Alteration in 5HT1A/2C and alpha2 receptors

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8
Q

What is the neuroendocrine hypothesis of depression?

A

-Changes in hypothalamic-pituitary-adrenal axis
-Stress causes hypothalamus to release CRF
-CRF promotes release of ACTH from pituitary
-ACTH promotes release of cortisol from adrenal
-Overactivity of HPA and elevated CRF found in almost all depressed patients
-Overactivity of HPA and elevated CRF found in almost all depressed patients
-Overactivity of HPA may desensitize feedback response in hypothalamus an pituitary
-Elevated CRF causes insomnia, anxiety, and decreased appetite and libido
-Antidepressants and ECT reduce CRF levels

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9
Q

What is the neurotrophic hypothesis of depression?

A

-Brain-derived neurotrophic factor is critical in neural plasticity, resilience, neurogenesis
-Stress and pain decrease BDNF levels in animals
-Decrease in volume of hippocampus
-BDNF has antidepressant activity in animals
-Depressed patients have reduced BDNF levels
-Antidepressants increase BDNF levels and may increase hippocampal volume

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10
Q

Which hypothesis of depression is correct?

A

All hypotheses can explain depression

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11
Q

What are the main classes of antidepressants?

A

-MAOIs
-TCAs
-SSRIs
-SNRIs
-5-HT2 antagonists
-Tetracyclic and unicyclic antidepressants

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12
Q

Why does antidepressant therapy take 2-3 weeks?

A

-Neuroadaptive responses?
-Activation of presynaptic receptors?
-Presynaptic adaptation?
-Postsynaptic adaptation?
-No one really knows

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13
Q

Mechanism of action of MAOIs

A

-Norepinephrine and serotonin are normally degraded by monoamine oxidase
-Blocking this degradation causes the vesicles to increase the amount of NE and 5HT that are packaged
-These vesicles then release more NE and 5HT into the synapse

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14
Q

What are the non-selective MAO inhibitors?

A

-Phenelzine
-Tranylcypromine

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15
Q

What are the MAO-B selective inhibitors?

A

-Selegiline

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16
Q

What are the MAO-A selective inhibitors?

A

-Moclobemide

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17
Q

What class of MAO inhibitors is irreversible?

A

Non-selective MAO inhibitors

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18
Q

What are common side effects associated with MAO inhibitors?

A

-Headache
-Drowsiness
-Dry mouth
-Weight gain
-Orthostatic hypotension
-Sexual dysfunction
-Hypertensive crisis

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19
Q

What are common interactions with MAOIs?

A

-Cold preparations and diet pills
-TCAs, SSRIs, L-DOPA
-Foods with tyramine
-St. Johns Wort

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20
Q

Indications for TCAs

A

-Depression
-Panic disorder
-Chronic pain
-Enuresis (bed wetting)

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21
Q

Overdose/toxic effects of TCAs

A

-Extremely dangerous, depressed patients are more likely to be suicidal
-Patients are more likely to commit self-harm or suicide 2 weeks into treatment

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22
Q

Tertiary amine mechanism of action

A

-Inhibits both NE and 5HT reuptake via NET and SERT
-Also acts as antagonists on H1 histamine receptors, muscarinic receptors, and alpha1 receptors

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23
Q

Major side effects associated with tertiary amines

A

-Sedation
-Autonomic side effects
-Weight gain
-Conduction disturbances of the heart (not major)

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24
Q

What are the tertiary amines used?

A

-Imipramine
-Amitriptyline
-Clomipramine (used for OCD)
-Doxepin

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25
Q

What is imipramine metabolized to?

A

Desipramine

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26
Q

What is amitriptyline metabolized to?

A

Nortriptyline

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27
Q

What are the secondary amines used?

A

-Desipramine
-Nortriptyline
-Maprotiline (NET inhibitor)

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28
Q

Side effects of secondary amines

A

Less sedation, anticholinergic effects, autonomic effects, weight gain, and cardiovascular effects compared to tertiary amines

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29
Q

What are the SSRIs used?

A

-Fluoxetine (little autonomic SE, no sedation)
-Fluvoxamine
-Paroxetine
-Sertraline
-Citalopram
-Escitalopram

30
Q

What are SSRIs used for?

A

-Depression
-Alcoholism
-OCD
-Enuresis
-PTSD
-Eating disorders
-Social phobias
-Panic anxiety
-PMDD
-GAD

31
Q

Side effects of SSRIs

A

-Nausea/vomiting
-Sexual dysfunction
-Anxiety
-Insomnia
-Tremors

32
Q

Side effects of abruptly discontinue SSRIs

A

-Brain zaps
-Dizziness
-Sweating
-Nausea
-Insomnia
-Tremor
-Confusion
-Vertigo

33
Q

What drugs can cause serotonin syndrome?

A

-MAOIs
-TCAs
-Metoclopramide
-Tramadol
-Triptans
-St. Johns Wort

34
Q

Symptoms of serotonin syndrome

A

-Hyperthermia
-Muscle rigidity
-Restlessness
-Myoclonus
-Hyperreflexia
-Sweating
-Shivering
-Seizures
-Coma

35
Q

How to treat serotonin syndrome

A

-Discontinuation of medication and management of symptoms
-Administration of serotonin antagonists (cyproheptadine or methysergide)
-Benzodiazepines to control myoclonus

36
Q

What are the SSRI+5HT1A partial agonists?

A

-Vilazodone
-Vortioxetine

37
Q

Differences between SSRI+5HT1A partial agonists and pure SSRIs

A

SSRI+5HT1A partial agonists have less sexual side effects vs pure SSRIs

38
Q

What are the tetracyclic and unicyclic antidepressants used?

A

-Maprotiline
-Mirtazipine
-Bupropion

39
Q

Maprotiline mechanism of action

A

NET inhibitor

40
Q

Mirtazapine mechanism of action

A

-Alpha2 antagonist
-5HT2 and 5HT3 antagonist
-H1 antagonist

41
Q

Bupropion mechanism of action

A

-DAT inhibitor
-NET and SERT inhibitor
-Also treats GAD
-Zyban for smoking cessation

42
Q

What are the 5-HT2 antagonists/SERT inhibitor?

A

Trazodone (Off-label hypnotic)

43
Q

What are the SNRIs?

A

-Venlafaxine
-Desvenlafaxine
-Duloxetine
-Milnacipran
-Levomilnacipran

44
Q

Venlafaxine clinical pearls

A

-NET and SERT inhibitor
-Treats GAD and panic disorder
-Diabetic neuropathy
-Migraine prophylaxis

45
Q

Desvenlafaxine clinical pearls

A

-NET and SERT inhibitor
-Approved by FDA February 2008
-Treatment of vasomotor symptoms associated with menopause?

46
Q

Duloxetine clinical pearls

A

-NET and SERT inhibitor
-Treats GAD
-Treats peripheral neuropathy

47
Q

Milnacipran clinical pearls

A

-NET and SERT inhibitor
-Approved for fibromyalgia

48
Q

Levomilnacipran clinical pearls

A

-Active enantiomer of milnacipran
-NET and SERT inhibitor
-Approved in 2013

49
Q

What are the norepinephrine selective reuptake inhibitors?

A

-Reboxetine
-Atomoxetine

50
Q

Reboxetine clinical pearls

A

-Possibly less side effects than Prozac
-Licensed in over 50 countries by 2007
-The FDA declined the license for use in the USA for unknown reasons

51
Q

Atomoxetine clinical pearls

A

-Originally intended to be an antidepressant drug (not approved!)
-Used for ADHD

52
Q

What are the serotonin-norepinephrine-dopamine reuptake inhibitors?

A

-Tesofensine
-Brasofensine

53
Q

What are triple blockers used for?

A

-Early research as Parkinson’s therapies
-Tesofensine is currently being researched as an appetite suppressants

54
Q

What are the NMDA antagonists?

A

-Ketamine - subanesthetic doses
-Scopolamine (muscarinic and NMDA antagonist)
-Lanicemine

55
Q

Esketamine side effects

A

-Depression
-Drug interactions

56
Q

How to treat postpartum depression

A

-SSRIs (fluoxetine and paroxetine)
-Venlafaxine
-CBT and counseling
-Brexanolone

57
Q

Brexanolone mechanism of action

A

-Allopregnanolone levels increase during pregnancy
-GABAa receptors desensitize
-Allopregnanolone levels return to normal postpartum
-Brexanolone resensitizes GABAa receptors

58
Q

New antidepressants in development

A

-Psychedelics: MDMA (ecstasy), psilocybin, and LSD (acid)
-5HT2C receptor antagonists
-Metabotropic glutamate receptor agonists
-Reversible inhibitors of monoamine oxidase-A (RIMAS)

59
Q

Non-pharmacologic considerations for treatment of depression

A

-Electroconvulsive therapy
-Psychotherapy
-Hospitalization

60
Q

Pharmacotherapeutic considerations

A

-Severity of depression
-Onset of drug action
-Endogenous vs exogenous depression
-Unipolar vs bipolar
-Drug selection
-Dosing
-Duration of therapy
-Compliance
-Other factors

61
Q

Pharmacology of Filbanserin

A

-Hypoactive sexual desire disorder
-Developed as antidepressant
-Polypharmacology - agonist at 5HT1A, antagonist at 5HT2A/C
-Regional selectivity - prefontal cortex
-Controversial approval

62
Q

Types of bipolar

A

-Bipolar 1 disorder
-Bipolar 2 disorder
-Cyclothymia disorder
-Unspecified bipolar and related disorder
-Substance-induced mood disorder

63
Q

Bipolar symptoms

A

-Mania
-Hypomania
-Depression
-Mixed mania and depression

64
Q

Symptoms of mania

A

-Euphoria/elation
-Irritability/anger
-Impulsive high risk behavior
-Aggressive
-Grandiose ideas
-Decrease sleep and appetite
-Difficulty concentrating
-Delusions
-Flight of ideas
-Hallucinations

65
Q

What is hypomania?

A

Less severe mania

66
Q

Treatments of bipolar disorder

A

-Hospitalization
-Psychotherapy
-Pharmacotherapy

67
Q

What drugs are used to treat bipolar disorder?

A

-Lithium
-Anticonvulsants
-Atypical antipsychotics
-Calcium-channel blockers (verapamil, nimopidine)
-Combo therapy (+BZD)

68
Q

Lithium clinical pearls

A

-Mechanism not clearly understood
-Deletion of PIP2 and associated signaling
-Modulate GSK3
-Small therapeutic index
-Acute vs chronic
-Lag time for effectiveness
-Loading dose

69
Q

Anticonvulsants used for depression

A

-Sodium valproate
-Carbamazepine
-Lamotrigine
-Topiramate

70
Q

Anticonvulsant mechanism of action

A

-Increase GABAergic tone (increase GAD activity, inhibit GABA transaminase)
-Block Na+ channels
-Block T-type Ca2+ channels
-Inhibits histone deacetylase (HADAC5)

71
Q

Atypical antipsychotics used for depression

A

-Olanzapine
-Olanzapine + fluoxetine
-Quetiapine
-Risperidone
-Ziprasidone
-Lurasidone
-Aripiprazole

Therapeutics III (42 decks)

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