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Pharmacology > Lecture 11 - Antidepressants > Flashcards

Lecture 11 - Antidepressants Flashcards

1
Q

Drugs used as antidepressants

A 
amitriptyline
imipramine
fluoxetine
paroxetine
sertraline
mirtazapine
buprorion
venlafaxine
phenelzine
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2
Q

List 3 types of depressive disorders

A

1 - reactive (secondary depression)

2 - bipolar disorder

3 - major depression

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3
Q

Describe:

1 - reactive (secondary depression)

A
  • temporary rxn to real stimuli such as grief or illness

- treatment is largely by psychotherapy

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4
Q

Describe:

2 - bipolar disorder

A

-recurrent major depressive episodes with intervening manic, hypomanic, or mixed episodes

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5
Q

Describe:

3 - major depression

A

-one or more major depressive episodes free of manic, mixed or hypomanic episodes

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6
Q

Lifetime prevalence in males?

A

9.6%

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7
Q

Lifetime prevalence in females?

A

20.4%

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8
Q

____% of the population are at risk of experience a major depressive episode at any given time

A

3-5

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9
Q

Onset?

A

most frequently 25-44 years of age

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10
Q

____ % have a single episode

A

30-50

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11
Q

recurrent episodes in ____%

A

50-70

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12
Q

If a first degree relative has depression, how much more likely are you to get depression?

A

1.5-3 times more likely

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13
Q

Risk of major depression determined by inheritance = ?

A

39%

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14
Q

Risk of major depression determined by environment = ?

A

61%

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15
Q

List the 4 types of symptoms of major depression

A

1-emotional
2-physical
3-cognitive
4-psychomotor

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16
Q

Describe:

1-emotional

A
  • diminished ability to experience pleasure
  • loss of interest in usual activities
  • pessimistic outlook
  • anxiety (90%)
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17
Q

Describe:

2-physical

A
  • chronic fatigue
  • terminal insomnia
  • appetite disturbances
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18
Q

Describe:

3-cognitive

A
  • poor concentration
  • slow thinking
  • poor short-term memory
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19
Q

Describe:

4-psychomotor

A
  • slowed physical movements and speech

- agitation

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20
Q

Diagnosis for depression?

A

have to have at least 5 symptoms of these over a period of 2 weeks to be diagnosed with depression

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21
Q

List 2 non-pharmacologic therapies for major depression

A
  • psychotherapy

- ECT (electroconvulsive therapy)

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22
Q

Describe pharmacologic therapy for major depression

A
  • 50-60% of Pts responsive
  • newer drugs well-tolerated and present little risk for OD
  • all drugs have similar efficacy
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23
Q

Describe the amine hypothesis

A

depression is related to reduced synaptic levels of NE and 5-HT

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24
Q

What supports the amine hypothesis?

A

1) 1950’s - Reserpine was proven to reduce NE and 5-HT metabolism and caused depression in 15% of patients
2) Most antidepressant drugs appear to work by enhancing synaptic monoamines (by blocking reuptake)

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25
Q

How long is the therapeutic lag for antidepressants?

A

1-4 weeks

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26
Q

Antidepressants have ___-term synaptic effects that influence synaptic strength

A

long

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27
Q

Describe Phase 1 amine enhancement

A

short-term (min-hrs)

uptake inhibition

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28
Q

Describe Phase 2 amine enhancement

A

long-term (weeks) effects of phase 1 enhancement - produces further enhanced amine levels to reach therapeutic significance

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29
Q

Explain “understand Phase 2”

A
  • normal scenario - pre-synaptic receptors that feedback inhibit to stop amine release
  • phase 1 causes homeostatic agonist down regulation of these receptors to maintain “normal” agonist:receptor interaction levels
  • results in reduced negative feedback and phase 2 amine increase
30
Q

Give examples of TCAs

A

**amitriptyline
**imipramine
clomipramine
doxepin
protriptyline
desipramine

**most important

31
Q

Describe the mechanism of how TCAs work

A

-mixed norepinephrine and serotonin reuptake inhibitors

32
Q

Other than depression, what else can TCAs be used for?

A

neuropathic pain

33
Q

TCAs also cause some blockade of ??

A

cholinergic, histaminergic, and alpha 1 adrenergic receptors

34
Q

What do the other blockades result in?

A

adverse effects

35
Q

Adverse effects of tricyclic antidepressants

A
  • antimuscarinic effects
  • cardiovascular (orthostatic hypotension, conduction defects)
  • sedation
  • sympathomimetic (tremor, insomnia)
  • neurologic - seizures
  • metabolic - weight gain, sexual disturbances
  • overdose - extremely dangerous cardiac arrhythmias
36
Q

Pharmacokinetic drug interactions

A

CYP 2D6 inhibitors

highly protein bound

37
Q

Pharmacodynamic drug interactions

A

sedatives

sympathomimetic antimuscarinic

38
Q

Describe a pharmacokinetic drug interaction

A

one drug affects the other’s absorption, distribution, metabolism, or excretion

39
Q

Describe a pharmacodynamic drug interaction

A

two drugs have additive or antagonistic effects

40
Q

Give examples of SSRIs

A

fluoxetine
paroxetine
sertraline
citalopram

41
Q

Describe the mechanism of SSRIs

A

-block serotonin reuptake 300-700 fold more effectively than NE

42
Q

Are SSRIs anymore effective than TCAs?

A

no

43
Q

Which 2 SSRIs have shorter half lives?

A

paroxetine

sertraline

44
Q

Which SSRI was used first?

A

fluoxetine

45
Q

_____ is most SERT-selective

A

citalopram

46
Q

Adverse effects of SSRIs

A
  • much less cholinergic, histaminergic, adrenergic receptor blockade than TCAs therefore more tolerable side effect profile (& better compliance)
  • safer in OD
  • associated with mild, short-lived GI symptoms, headache
  • sexual dysfunction, fatigue, insomnia
  • paroxetine withdrawl can cause dizziness, nausea, tremor, anxiety
  • platelet inhibition
47
Q

Pharmacokinetic drug interactions

A
  • Strong CYP 2D6 inhibitors
  • TCAs
  • antipsychotics
  • B blockers interfere with metabolism
48
Q

Pharmacodynamic drug interactions

A

low non-SERT interactions

49
Q

Describe advantages of SSRIs over TCAs (3)

A
  • equal efficacy with milder side effect profile
  • much more favourable therapeutic index
  • smaller chance of additive drug interactions (ex. anticholinergic)
50
Q

Examples of SNRIs

A

venlafaxine
duloxetine
desvenlafaxine

51
Q

Describe the mechanism of SNRIs

A

inhibit both serotonin and NE reuptake (5-HT>NE)

also weak dopamine reuptake inhibitors

no affinity for muscarinic, alpha 1 adrenergic or histaminergic receptors

52
Q

Adverse effects of SNRIs

A
  • similar to SSRIs
  • much lower incidence than TCAs

Adverse effects can include:

  • nausea
  • sweating
  • dizziness
  • anxiety
  • sexual dysfunction
  • hypertension
53
Q

Pharmacodynamic drug interactions for SNRIs?

A

limited

54
Q

other drug interactions for SNRIs

A

protein binding varies:

  • venlafaxine (30%)
  • duloxetine (>90%)

CYP 2D6 substrate (venlafaxine, duloxetine)

55
Q

Potential advantages of SNRIs over TCAs

A
  • same milder side effect profile as SSRIs
  • may be useful for depression with neuropathic pain
  • fewer drug interactions
  • potentially lower safety margin than SSRIs in OD
56
Q

Mirtazapine (Remeron) is an ??

A

atypical antidepressant

57
Q

Describe the mechanism of mirtazapine

A
  • blocks the alpha 2 adrenergic receptors thus increasing NE release
  • has low affinity for muscarinic and alpha 1 adrenergic receptors
  • potent blocker of histamine receptors
58
Q

Adverse effects of mirtazapine

A

sedation
weight gain

no anticholinergic effects

less propensity for sexual side effects than SSRIs and TCAs

59
Q

Any drug interactions for atypical antidepressants?

A

none known

60
Q

Advantages of mirtazapine?

A
  • they are as tolerable as SSRIs
  • anxiolytic/sedative effect can be useful
  • antihistamine
  • minimal cholinergic/adrenergic drug interactions
61
Q

Major draw back of using mirtazapine?

A

weight gain

IMPORTANT POINT

62
Q

Mechanism of Buproprion

A

largely unknown!

  • does not inhibit NE or serotonin reuptake
  • weakly blocks dopamine reuptake
  • mild stimulant - treats comorbid fatigue/poor concentration, ADHD
  • low affinity for muscarinic, alpha 1 adrenergic or histaminergic receptors
63
Q

Adverse effects of buproprion

A
  • much lower incidence than TCAs
  • can include nausea, headache, dizziness, insomnia, seizures

**no sexual dysfunction or weight gain or sedation

64
Q

Drug interactions with bupropion

A
  • meds that lower seizure threshold, L-dopa

- CYP 2D6 inhibitor

65
Q

Advantages of bupropion

A
  • as tolerable as SSRIs
  • stimulant effects may be helpful
  • may offer relief from SSRI or SNRI-induced sexual dysfunction or weight gain
66
Q

Examples of monoamine oxidase inhibitors (MAOIs)

A

phenelzineu
moclobemide
tranylcypromine

67
Q

explain the mechanism of MAOIs

A

MAO-A breaks down NE and serotonin

MAO-B breaks down dopamine

we are inhibiting these so therefore we would increase NE, serotonin, and dopamine

68
Q

When would you use MAOIs?

A

they are usually reserved for patients unresponsive to other therapies due to side effects and drug and food interactions

*def not 1st line treatment

69
Q

Adverse effects of MAOIs

A
  • orthostatic hypotension
  • antimuscarinic
  • mild-moderate sedation
  • dose-related sexual dysfunction in males and females
  • hypertensive crisis
70
Q

see slide 28

A

kay man

71
Q

What 2 types of antidepressants are first line therapies?

A

SSRI

SNRI

Pharmacology (21 decks)

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