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PHAC II > 8. Antidepressants > Flashcards

8. Antidepressants Flashcards

1
Q

What are the 5 different classes of antidepressants?

A
  1. MAOIs
  2. TCAs
  3. SSRIs
  4. SNRIs
  5. Atypicals
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2
Q

What is reactive depression?

A
  • temporary reaction to real stimuli such as grief or illness
  • treatment is mainly psychotherapy
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3
Q

What is bipolar disorder?

A
  • recurrent major depressive episodes with intervening manic, hypomanic or mixed episodes.
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4
Q

What is major depression?

A
  • one or more major depressive episodes free of manic, mixed or hypomanic episodes.
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5
Q

Is major depression more prevalent in males or females

A

Females

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6
Q

What are the 4 symptom categories of major depression?

A
  1. Emotional
  2. Physical
  3. Cognitive
  4. Psychomotor
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7
Q

What are the physical sx of major depression?

A
  • chronic fatigue
  • terminal insomnia
  • appetite disturbances
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8
Q

What are the cognitive sx of major depression?

A
  • poor concentration
  • slow thinking
  • poor short-term memory
  • confusion
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9
Q

What are the psychomotor sx of major depression?

A
  • slowed physical movements and speech

- agitation

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10
Q

What are the non-pharmacologic therapies for major depression?

A
  • psychotherapy

- ECT

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11
Q

What is the amine hypothesis?

A

It is the theory that depression is related to reduced synaptic levels of NE and 5HT (serotonin)

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12
Q

How do most antidepressants enhance synaptic monoamines?

A

By blocking normal NT reuptake processes, NET and SERT.

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13
Q

What is therapeutic lag?

A

The period of time it takes for antidepressants to actually create a noticeable effect (~ 1-4 weeks)

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14
Q

Describe the phases that take place in presynaptic autoreceptor downregulation.

A

Phase 1

  • short term
  • uptake inhibition

Phase 2

  • long term effect of phase 1 enhancement
  • this produces enhanced amine levels to reach therapeutic significance
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15
Q

How does phase 1 enhance phase 2 with respect to receptor downregulation?

A
  • phase 1 causes homeostatic downregulation of the receptors to maintain “normal” agonist:receptor interaction levels
  • this results in reduced negative feedback and phase 2 amine increase
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16
Q

What is directly related to how many presynaptic receptors are downregulated?

A

improved mood

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17
Q

What is the MOA of TCAs?

A
  • mixed NE and 5HT reuptake inhibitors
  • great variation in the ratio of inhibition
  • also used in neuropathic pain (due to NET effect)
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18
Q

What are the side effects of TCAs?

A
  • antimuscarinic
  • cardiovascular
  • sedation
  • sympathomimetic
  • neurologic (seizures)
  • metabolic
  • OD (dangerous arrhythmias)
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19
Q

What are the PK drug interactions produced by TCAs?

A
  • inhibits CYP 2D6

- highly protein bound –> can displace other protein bound drugs

20
Q

What are the PD drug interactions produced by TCAs?

A

Increases the effects of sedatives, sympathomimetics and antimuscarinics?

21
Q

Explain the MOA of SSRIs.

A
  • blocks serotonin reuptake very strongly (much more than NE)
  • increases levels of 5HT in the synapse
22
Q

What are 3 examples of SSRIs?

A
  • fluoxetine
  • paroxetine
  • sertraline
23
Q

What are the SEs associated with SSRIs?

A
  • mild GI sx
  • headache
  • sexual dysfunction
  • insomnia
  • platelet aggregation inhibition (clotting issues)
24
Q

Why do SSRIs and SNRIs have a better SE profile?

A

because they have little or no affinity for the cholinergic, histaminergic or adrenergic receptors –> less SE

25
What are the PK drug interactions associated with SSRIs?
- strongly inhibit CYP 2D6 | - TCAs, antipsychotics, beta blockers interfere with metabolism
26
Why should a pt not abruptly discontinue using paroxetine? What are the sx?
- pt could experience paroxetine withdrawal - due to low half life of paroxetine - dizziness, nausea, tremor, anxiety
27
What are the PD drug interactions associated with SSRIs?
- Low chances | - Low non-SERT interactions
28
What are 3 advantages of SSRIs over TCAs?
1. equal efficacy with milder SEs 2. Better therapeutic index 3. smaller chance of additive drug interaction (low affinity for other receptors)
29
Explain the MOA of SNRIs
- inhibit both 5HT and NE reuptake (similar to TCAs) - also weak dopamine reuptake inhibitor - no affinity for other receptors (less SEs)
30
What are the SEs of SNRIs?
- nausea - sweating - dizziness - anxiety - sexual dysfunction - HTN - might be more dangerous than SSRIs in OD
31
Give an example of a SNRI
Venlafaxine
32
What are 3 advantages of SNRIs of SSRIs/TCAs? | Disadvantage?
- same milder SEs as SSRIs - may be useful for depression with neuropathic pain (NE effects) - fewer drug interactions - more dangerous OD potential that SSRIs
33
Mirtazapine is an atypical antidepressant. What is its MOA?
- block alpha 2 adrenergic receptors --> increases NE release - low affinity for muscarine and alpha 1 receptors - potent blocker of histamine receptors
34
Give an example of an atypical antidepressant.
Mirtazapine | Bupropion
35
What are the side effects of Mirtazapine?
- sedation - weight gain - less sexual SEs than SSRIs/TCAs - no anticholinergic effects
36
What drug interactions are associated with MIrtazapine?
none are known
37
Explain buproprion's MOA.
- unknown (doesn't inhibit NE or 5HT reuptake) - weakly block dopamine reuptake - mild stimulant (helps fatigue, poor concentration, ADHD)
38
What are the SEs associated with buproprion?
- much less than TCAs - nausea - headache - dizziness - insomnia - seizures - NO sexual dysfunction - weight gain - sedation
39
What are the drug interactions associated with buproprion?
- L-Dopa - meds that lower seizure threshold (increased seizure risk) - CYP 2D6 inhibitor
40
What are the advantages of buproprion?
- as tolerable as SSRIs - stimulant effects may be helpful - may offer relief from sexual dysfunction or weight gain from SSRI/SNRI use
41
Explain the MOA of MAOIs.
- MAO-a breaks down NE and 5HT, MAO-b break down dopamine --> MAOIs stop this
42
When are MAOIs prescribed?
when pts are unresponsive to other therapies | due to SEs, drug/food interactions with other antidepressants
43
Give an example of a MAOI.
Phenelzine
44
What are the SEs of MAOIs?
- orthostatic hypotension | - antimuscarinic (
45
What are the drug interactions associated with MAOIs?
Serotonine syndrome when combined with 5HT R.I. (TCA, SSRI, SNRI) - hyperthermia, mania, muscle rigidity can develop - can be lethal...need 2-5 weeks of washout

PHAC II (9 decks)

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