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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
Escitalopram uses (in addition to depression)
General anxiety disorder
26
Fluoxetine indications (other than anti-depressant)
1. Obsessive compulsive disorder 2. Bulimia nervosa 3. Panic disorder
27
Fluoxetine + **Olanzapine** indications (2) (other than anti-depressant)
1. Acute depressive episodes associated with bipolar 1 disorder 2. Acute treatment of treatment-resistant depression
28
Paroxetine indications (other than antidepressant)
1. Premenstrual dysmorphic disorder 2. Panic disorder
29
SSRI inhibits one or more cytochrome p450 drug metabolizing enzyme. Pharmacokinetic interactions are seen between which two antidepressants?
* Tamoxifen AND * Fluoxetine or Paroxetine
30
Which 2 SSRIs have little to no inhibition of CYP450?
1. Citalopram 2. Escitalopram
31
Pregnancy : Fluoxetine appears to be safe while ______ may be associated with an increased risk of congenital heart defects
paroxetine
32
SSRI class effects
asthenia (also...diaphoresis, diarrhea, hyperprolactinemia, SIADH and hyponatremia)
33
Sertraline side effect
diarrhea (all drugs may cause this)
34
Ctialopram side effects
dose-dependent QT interval prolongation
35
Escitalopram side effects
prolong the corrected QT interval
36
Paroxetine side effect
* weight gain * sexual dysfunction * cardiac septal defects if taken in first trimester
37
Serotonin syndrome
Increase serotonergic activity in the CNS (serotonin is involved in regulating GI motility, vasoconstriction, uterine contraction and bronchoconstriction)
38
Serotonin syndrome treatment
Sedation with benzodiazepine (Cyproheptadine if this fails - H1 receptor antagonist for 5-HT1A & 5-HT2A antagonist)
39
If the patient has been an adequate response or intolerable side effects during the first line treatment with SSRIs, _____ (2 alternative antidepressants)
1. Bupoprion 2. Mirtazapine
40
Bupropion (aka WELLBUTRIN) indications
1. Depression 2. Tobacco dependence (off label for SAD, ADD, obesity)
41
Bupropion (aka WELLBUTRIN) mechanism of action
Presynaptic uptake of DA and NE (greater on DA)
42
Bupropion (aka WELLBUTRIN) contraindications
1. Bulimia nervosa 2. Anorexia nervosa 3. Seizure disorder 4. Abrupt withdrawal from alcohol, benzos are other sedatives
43
Bupropion (aka WELLBUTRIN) adverse effects
1. Seizures 2. Mildly stimulating (May benefit patients with fatigue, hypersomnia or poor concentration) 3. **Insomnia & agitation**
44
Mirtazapine indications
1. Depression 2. Sedation (helpful for patients with insomnia)
45
Mirtazapine MOA (2)
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
Mirtazapine side effects
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
Fluvoxamine indication (other than anti-depressant)
OCD
48
Metabolism of each SSRI except for _____ produces active metabolites.
fluvoxamine (prodrug) (fluoxetine yields norfluoxetine with is an SSRI)
49
Fluoxetine is metabolized to \_\_\_\_\_\_\_.
norfluoxetine (SSRI)
50
The elimination half-life for ssris is approximately \_\_\_\_\_
20-30 hours (except for fluoxetine and fluvoxamine)
51
Half-life for Fluoxetine. Fluvoxamine half life
1. Fluoxetine: 1-3 days (norfluoxetine 4-16 days) 2. Fluvoxamine: 15 hours
52
Buproprion metabolism (active metabolite, inhibition)
1. Hydroxybupropion 2. Inhibits CYP2D6 (dose adjustment may be needed for renal or liver disease pts)
53
In addition to depression, **Sertraline** also treats \_\_\_\_\_\_(5).
1. OCD 2. Panic disorder 3. PMDD 4. PTSD 5. Social Anxiety 6.
54
Define asthenia
daytime sedation with malaise, diminished mental energy or emotional blunting
55
Paroxetine & fluvoxamine are known to cause _______ which two side effects?
1. Nausea 2. Sedation

Behavioral Medicine (35 decks)

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