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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
How long is the therapeutic lag for antidepressants?
1-4 weeks
26
Antidepressants have ___-term synaptic effects that influence synaptic strength
long
27
Describe Phase 1 amine enhancement
short-term (min-hrs) | uptake inhibition
28
Describe Phase 2 amine enhancement
long-term (weeks) effects of phase 1 enhancement - produces further enhanced amine levels to reach therapeutic significance
29
Explain "understand Phase 2"
- 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
Give examples of TCAs
**amitriptyline **imipramine clomipramine doxepin protriptyline desipramine **most important
31
Describe the mechanism of how TCAs work
-mixed norepinephrine and serotonin reuptake inhibitors
32
Other than depression, what else can TCAs be used for?
neuropathic pain
33
TCAs also cause some blockade of ??
cholinergic, histaminergic, and alpha 1 adrenergic receptors
34
What do the other blockades result in?
adverse effects
35
Adverse effects of tricyclic antidepressants
- antimuscarinic effects - cardiovascular (orthostatic hypotension, conduction defects) - sedation - sympathomimetic (tremor, insomnia) - neurologic - seizures - metabolic - weight gain, sexual disturbances - overdose - extremely dangerous cardiac arrhythmias
36
Pharmacokinetic drug interactions
CYP 2D6 inhibitors | highly protein bound
37
Pharmacodynamic drug interactions
sedatives | sympathomimetic antimuscarinic
38
Describe a pharmacokinetic drug interaction
one drug affects the other's absorption, distribution, metabolism, or excretion
39
Describe a pharmacodynamic drug interaction
two drugs have additive or antagonistic effects
40
Give examples of SSRIs
fluoxetine paroxetine sertraline citalopram
41
Describe the mechanism of SSRIs
-block serotonin reuptake 300-700 fold more effectively than NE
42
Are SSRIs anymore effective than TCAs?
no
43
Which 2 SSRIs have shorter half lives?
paroxetine | sertraline
44
Which SSRI was used first?
fluoxetine
45
_____ is most SERT-selective
citalopram
46
Adverse effects of SSRIs
- 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
Pharmacokinetic drug interactions
- Strong CYP 2D6 inhibitors - TCAs - antipsychotics - B blockers interfere with metabolism
48
Pharmacodynamic drug interactions
low non-SERT interactions
49
Describe advantages of SSRIs over TCAs (3)
- equal efficacy with milder side effect profile - much more favourable therapeutic index - smaller chance of additive drug interactions (ex. anticholinergic)
50
Examples of SNRIs
venlafaxine duloxetine desvenlafaxine
51
Describe the mechanism of SNRIs
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
Adverse effects of SNRIs
- similar to SSRIs - much lower incidence than TCAs Adverse effects can include: - nausea - sweating - dizziness - anxiety - sexual dysfunction - hypertension
53
Pharmacodynamic drug interactions for SNRIs?
limited
54
other drug interactions for SNRIs
protein binding varies: - venlafaxine (30%) - duloxetine (>90%) CYP 2D6 substrate (venlafaxine, duloxetine)
55
Potential advantages of SNRIs over TCAs
- 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
Mirtazapine (Remeron) is an ??
atypical antidepressant
57
Describe the mechanism of mirtazapine
- 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
Adverse effects of mirtazapine
sedation weight gain no anticholinergic effects less propensity for sexual side effects than SSRIs and TCAs
59
Any drug interactions for atypical antidepressants?
none known
60
Advantages of mirtazapine?
- they are as tolerable as SSRIs - anxiolytic/sedative effect can be useful - antihistamine - minimal cholinergic/adrenergic drug interactions
61
Major draw back of using mirtazapine?
weight gain IMPORTANT POINT
62
Mechanism of Buproprion
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
Adverse effects of buproprion
- much lower incidence than TCAs - can include nausea, headache, dizziness, insomnia, seizures **no sexual dysfunction or weight gain or sedation
64
Drug interactions with bupropion
- meds that lower seizure threshold, L-dopa | - CYP 2D6 inhibitor
65
Advantages of bupropion
- as tolerable as SSRIs - stimulant effects may be helpful - may offer relief from SSRI or SNRI-induced sexual dysfunction or weight gain
66
Examples of monoamine oxidase inhibitors (MAOIs)
phenelzineu moclobemide tranylcypromine
67
explain the mechanism of MAOIs
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
When would you use MAOIs?
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
Adverse effects of MAOIs
- orthostatic hypotension - antimuscarinic - mild-moderate sedation - dose-related sexual dysfunction in males and females - hypertensive crisis
70
see slide 28
kay man
71
What 2 types of antidepressants are first line therapies?
SSRI | SNRI

Pharmacology (21 decks)

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