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Behavioral Medicine > Anti-depressants > Flashcards

Anti-depressants Flashcards

1
Q

Monoamine hypothesis

A

Generally a consistenet deficiency in the monoaminergic NTs (NE & 5-HT)

(functional deficiency = how much is available at the synapse, can neurotransmission be maintained by the amount that is there?)

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2
Q

only ______% of patients responsd to anti-depressants

A

40-50

(most end up on combination drugs)

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3
Q

What are the top drugs used in households?

A
  1. Sertraline
  2. Escitalopram
  3. Fluoxetine

(antidepressants)

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4
Q

The last antidepressant was developed in _____.

A

1990

(they’ve been around since the 50’s. They are the most used drugs, says a lot about how we are doing w/mental health)

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5
Q

______ helps with neural plasticity.

A

Psychedelics - use must be monitored by physicians

(sprouts new dendrites. These will likely be used in psychiatry soon. research trials are increasing)

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6
Q

What are some substances being researched for future depression treatment?

A
  1. NO
  2. Psychodelics (psilocybin)
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7
Q

Most common mood disorders

A
  1. Depression
  2. Bipolar disorder
  3. Seasonal affective disorder (SAD)
  4. Self-harm
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8
Q

Reserpine: MOA

A

blocks VAMT → inhibits NE re-uptake

(depletion of monoamine & symptoms of depression)

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9
Q

Iproniazid: MOA

A

inhibits MAO (monoamine oxidaze) enzymes

(alleviates symptoms of depression)

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10
Q

Limitations of the monoamine hypothesis of depression

A
  1. Therapeutic lag for up to 1 month
  2. No scientific basis for depletion / lack of NTs
  3. Hippocampal atrophy and loss of BDNF (brain derived neurotropic factor - food for the brain)
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11
Q

Serotonin promotes neurogenesis through ____ during depression and may underlie the beneficial effect of certain antidepressants.

A

BDNF

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12
Q

Rapid relief of depressive symptoms with ______.

A

Ketamine

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13
Q

Stress hypothesis of depression (3)

A
  1. Chronically elevated levels of glucocorticoids limits transcription and translation of BDNF (brain food)
  2. Thyroid dysregulation→ increases thyroxine
  3. Estrogen & testosterone decreases

(loss of dendritic sprouts, decreased TH4)

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14
Q

Why is there a therapeutic lag with antidepressants?

A

It takes time to increase the transcription of “brain food” (BDNF)

(note how cortisol inhibits this process)

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15
Q

Comorbidities of antidepressants

A
  1. Smoking cessation
  2. Epilepsy or bulimia
  3. Chronic pain
  4. Anxiety

(antidepressants may also treat these conditions)

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16
Q

Bupropion treats depression & ______.

A
  • smoking cessation
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17
Q

SNRI’s & TCAs treat depression & also ______ .

A
  • chronic pain (fibromyalgia & diabetic peripheral neuropathy)
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18
Q

SNRI & TCA pain modulation MOA

A

Facilitate descending pain modulation at second and first order neurons

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19
Q

Which antidepressant is being used to treat covid symptoms?

A

Fluvoxamine

(prevents cytokine storm)

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20
Q

Considerations in prescribing antidepressants

A
  1. Sexual dysfunction
  2. Weight gain
  3. Hypertension (SNRI’s)
  4. Bipolar

(this is especially important for PCP’s to understand)

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21
Q

______ (2) antidepressant types that increase the incidence of sexual dysfunction

A
  1. SSRI
  2. SNRI

(bupropion does not cause this, and actually may alleviate it)

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22
Q

Antidepressant that may increase the risk of hypertension

A

SNRI

(it basically activates the sympathetic nervous system)

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23
Q

______ (drug therapy) should be avoided in bipolar patients

A

anti-depressants monotheray

(it may cause rapid cycling & polarity switch)

24
Q

SSRI MOA

A

Allostericlly inhibits the transporter by binding to SERT receptor at the site other than serotonin binding site

25
Q

Escitalopram uses (in addition to depression)

A

General anxiety disorder

26
Q

Fluoxetine indications (other than anti-depressant)

A
  1. Obsessive compulsive disorder
  2. Bulimia nervosa
  3. Panic disorder
27
Q

Fluoxetine + Olanzapine indications (2) (other than anti-depressant)

A
  1. Acute depressive episodes associated with bipolar 1 disorder
  2. Acute treatment of treatment-resistant depression
28
Q

Paroxetine indications (other than antidepressant)

A
  1. Premenstrual dysmorphic disorder
  2. Panic disorder
29
Q

SSRI inhibits one or more cytochrome p450 drug metabolizing enzyme. Pharmacokinetic interactions are seen between which two antidepressants?

A
  • Tamoxifen

AND

  • Fluoxetine or Paroxetine
30
Q

Which 2 SSRIs have little to no inhibition of CYP450?

A
  1. Citalopram
  2. Escitalopram
31
Q

Pregnancy : Fluoxetine appears to be safe while ______ may be associated with an increased risk of congenital heart defects

A

paroxetine

32
Q

SSRI class effects

A

asthenia

(also…diaphoresis, diarrhea, hyperprolactinemia, SIADH and hyponatremia)

33
Q

Sertraline side effect

A

diarrhea

(all drugs may cause this)

34
Q

Ctialopram side effects

A

dose-dependent QT interval prolongation

35
Q

Escitalopram side effects

A

prolong the corrected QT interval

36
Q

Paroxetine side effect

A
  • weight gain
  • sexual dysfunction
  • cardiac septal defects if taken in first trimester
37
Q

Serotonin syndrome

A

Increase serotonergic activity in the CNS

(serotonin is involved in regulating GI motility, vasoconstriction, uterine contraction and bronchoconstriction)

38
Q

Serotonin syndrome treatment

A

Sedation with benzodiazepine

(Cyproheptadine if this fails - H1 receptor antagonist for 5-HT1A & 5-HT2A antagonist)

39
Q

If the patient has been an adequate response or intolerable side effects during the first line treatment with SSRIs, _____ (2 alternative antidepressants)

A
  1. Bupoprion
  2. Mirtazapine
40
Q

Bupropion (aka WELLBUTRIN) indications

A
  1. Depression
  2. Tobacco dependence

(off label for SAD, ADD, obesity)

41
Q

Bupropion (aka WELLBUTRIN) mechanism of action

A

Presynaptic uptake of DA and NE (greater on DA)

42
Q

Bupropion (aka WELLBUTRIN) contraindications

A
  1. Bulimia nervosa
  2. Anorexia nervosa
  3. Seizure disorder
  4. Abrupt withdrawal from alcohol, benzos are other sedatives
43
Q

Bupropion (aka WELLBUTRIN) adverse effects

A
  1. Seizures
  2. Mildly stimulating (May benefit patients with fatigue, hypersomnia or poor concentration)
  3. Insomnia & agitation
44
Q

Mirtazapine indications

A
  1. Depression
  2. Sedation (helpful for patients with insomnia)
45
Q

Mirtazapine MOA (2)

A
  1. Antagonist presynaptic Alpha 2 adrenergic receptors and postsynaptic serotonin receptors (5-HT2A, 5-HT2C & 5-HT3)
  2. High affinity for histamine H1 receptors (Sedating effect)
46
Q

Mirtazapine side effects

A
  1. Drowsiness (the most of the SSRIs)
  2. Agranulocytosis and neutropenia
  3. Increased appetite
  4. Weight gain

(dose may need to be adjusted for pts w/renal or liver dz)

47
Q

Fluvoxamine indication (other than anti-depressant)

A

OCD

48
Q

Metabolism of each SSRI except for _____ produces active metabolites.

A

fluvoxamine (prodrug)

(fluoxetine yields norfluoxetine with is an SSRI)

49
Q

Fluoxetine is metabolized to _______.

A

norfluoxetine (SSRI)

50
Q

The elimination half-life for ssris is approximately _____

A

20-30 hours

(except for fluoxetine and fluvoxamine)

51
Q

Half-life for Fluoxetine. Fluvoxamine half life

A
  1. Fluoxetine: 1-3 days (norfluoxetine 4-16 days)
  2. Fluvoxamine: 15 hours
52
Q

Buproprion metabolism (active metabolite, inhibition)

A
  1. Hydroxybupropion
  2. Inhibits CYP2D6

(dose adjustment may be needed for renal or liver disease pts)

53
Q

In addition to depression, Sertraline also treats ______(5).

A
  1. OCD
  2. Panic disorder
  3. PMDD
  4. PTSD
  5. Social Anxiety
    6.
54
Q

Define asthenia

A

daytime sedation with malaise, diminished mental energy or emotional blunting

55
Q

Paroxetine & fluvoxamine are known to cause _______ which two side effects?

A
  1. Nausea
  2. Sedation

Behavioral Medicine (35 decks)

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