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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
Q

What are the PK drug interactions associated with SSRIs?

A
  • strongly inhibit CYP 2D6

- TCAs, antipsychotics, beta blockers interfere with metabolism

26
Q

Why should a pt not abruptly discontinue using paroxetine? What are the sx?

A
  • pt could experience paroxetine withdrawal
  • due to low half life of paroxetine
  • dizziness, nausea, tremor, anxiety
27
Q

What are the PD drug interactions associated with SSRIs?

A
  • Low chances

- Low non-SERT interactions

28
Q

What are 3 advantages of SSRIs over TCAs?

A
  1. equal efficacy with milder SEs
  2. Better therapeutic index
  3. smaller chance of additive drug interaction (low affinity for other receptors)
29
Q

Explain the MOA of SNRIs

A
  • inhibit both 5HT and NE reuptake (similar to TCAs)
  • also weak dopamine reuptake inhibitor
  • no affinity for other receptors (less SEs)
30
Q

What are the SEs of SNRIs?

A
  • nausea
  • sweating
  • dizziness
  • anxiety
  • sexual dysfunction
  • HTN
  • might be more dangerous than SSRIs in OD
31
Q

Give an example of a SNRI

A

Venlafaxine

32
Q

What are 3 advantages of SNRIs of SSRIs/TCAs?

Disadvantage?

A
  • 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
Q

Mirtazapine is an atypical antidepressant. What is its MOA?

A
  • block alpha 2 adrenergic receptors –> increases NE release
  • low affinity for muscarine and alpha 1 receptors
  • potent blocker of histamine receptors
34
Q

Give an example of an atypical antidepressant.

A

Mirtazapine

Bupropion

35
Q

What are the side effects of Mirtazapine?

A
  • sedation
  • weight gain
  • less sexual SEs than SSRIs/TCAs
  • no anticholinergic effects
36
Q

What drug interactions are associated with MIrtazapine?

A

none are known

37
Q

Explain buproprion’s MOA.

A
  • unknown (doesn’t inhibit NE or 5HT reuptake)
  • weakly block dopamine reuptake
  • mild stimulant (helps fatigue, poor concentration, ADHD)
38
Q

What are the SEs associated with buproprion?

A
  • much less than TCAs
  • nausea
  • headache
  • dizziness
  • insomnia
  • seizures
  • NO sexual dysfunction
  • weight gain
  • sedation
39
Q

What are the drug interactions associated with buproprion?

A
  • L-Dopa
  • meds that lower seizure threshold (increased seizure risk)
  • CYP 2D6 inhibitor
40
Q

What are the advantages of buproprion?

A
  • as tolerable as SSRIs
  • stimulant effects may be helpful
  • may offer relief from sexual dysfunction or weight gain from SSRI/SNRI use
41
Q

Explain the MOA of MAOIs.

A
  • MAO-a breaks down NE and 5HT, MAO-b break down dopamine –> MAOIs stop this
42
Q

When are MAOIs prescribed?

A

when pts are unresponsive to other therapies

due to SEs, drug/food interactions with other antidepressants

43
Q

Give an example of a MAOI.

A

Phenelzine

44
Q

What are the SEs of MAOIs?

A
  • orthostatic hypotension

- antimuscarinic (

45
Q

What are the drug interactions associated with MAOIs?

A

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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