Lecture 11 - Antidepressants Flashcards Preview

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Flashcards in Lecture 11 - Antidepressants Deck (71)
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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