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.Pharmacology > Chapter 16: Antidepressant Drugs > Flashcards

Chapter 16: Antidepressant Drugs Flashcards

1
Q

depression is a complex ___ of conditions

A

spectrum

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2
Q

t/f non-harm treatments for depression are very important

A

true

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3
Q

___depressive disorder is the primary indication for antidepressants

A

major

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4
Q

what are some symptoms of major depressive disorder?

A

loss of interest/pleasure in normal activities; sleep/attitude disturbances; thoughts of guilt, worthlessness, suicide

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5
Q

t/f the pathologic causes of depression and why these symptoms arise is not clearly defined

A

true

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6
Q

what are the 2 most widely accepted theories of the pathology of depression?

A
  1. neurotrophic hypothesis

2. monoamine hypothesis

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7
Q

the neurotrophic hypothesis theory of depression suggests that depression is caused by a lack of ___ in he CNS

A

Brain-derived neurotrophic factor (BDNF)

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8
Q

a decrease in BDNF may lead to ___neuronal signalling and ___remodelling

A

reduced; brain

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9
Q

BDNF is an important factor in ____ and maintaining ___

A

neuroplasticicty; neuronal signalling

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10
Q

the monoamine theory of depression suggests that reduced levels of __, ___ and ___ (NT) in the ___ and __ sytstems of the brain cause depression

A

5-HT, DA, NE ; cortical and limbic

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11
Q

the greatest support for the monoamine theory of depression is that all available antidepressants increase ___ in the brain

A

monoamine levels

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12
Q

what is the greatest criticism for the monoamine theory of depression?

A

the long time taken for drugs to be effective

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13
Q

most treatments with antidepressants take ___(time) to become effective

A

4-6 weeks

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14
Q

t/f the roles of glutamate and other hormones have been suggested to be important to depression, but these role are less clear than the other theories

A

t

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15
Q

t/f it is lily that many factors contribute to depression and treatment should be personalized and it may take several trials before the best therapy is found

A

t

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16
Q

all antidepressants enhance monoamine transmission by one of 3 ways: ___, ___ and ___

A
  1. preventing reuptake
  2. enhancing release
  3. reducing their breakdown
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17
Q

the most common MOA for antidepressants is to inhibit the activity of ___, ___ or both to reduce NT reuptake

A

SERT, NET

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18
Q

Mirtazapine works as an antidepressant by… (MOA)

A

enhancing monoamine release by blocking presynaptic auto receptors or inhibiting break down

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19
Q

what would be the impact on levels of 5-HT, NE and DA if the monoamine oxidase was inhibited?

A

levels would rise

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20
Q

give 3 classes of drugs that reduce depression by preventing NT reuptake

A

SSRI; SNRI; TCA

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21
Q

monoamine oxidase inhibitors work by … (MOA)

A

preventing NT breakdown by MAO

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22
Q

___ and ___ class drugs are the most commonly used in depression

A

5-HT and NE reuptake inhibitors

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23
Q

___ is the transporter responsible for returning NE into the presynaptic neuron

A

NET

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24
Q

___ is the transporter of serotonin

A

SERT

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25
Q

fluoxetine MOA:

A

selectively blocks SERT so only 5-HT levels increase in the synapse

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26
Q

what class of drug is fluoxetine?

A

SSRI

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27
Q

does fluoxetine have any impact on NE?

A

no

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28
Q

SNRIs and TCAs target both ___ and ___

A

SERT and NET

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29
Q

SNRIs and TCAs reduce the re-uptake of both ___ and __

A

serotonin and NE

30
Q

Venlafaxine is a ____(drug class)

A

SNRIs

31
Q

which has fewer off-target effects, SNRIs or TCAs?

A

SNRIs

32
Q

most of the side effects that occur with SNRIs are related to

A

elevated NE and 5-HT levels

33
Q

amitriptyline is a ____ (drug Class)

A

TCA

34
Q

why are there more side effects associated with TCAs?

A

they have significant binding to other receptors

35
Q

what are 3 off-target receptors that TCAs bind to?

A

muscarinic; alpha 1 adrenergic, H1

36
Q

what type of auto receptors are booked by mirtazapine?

A

alpha 2

37
Q

when auto receptors are activated a ___coupled signalling cascade occurs, which ____(increases/decreases) the NT releases

A

Gi; decreases

38
Q

what is an off-target receptor that mirtzapine binds strongly to?

A

H1 (blocks histamine)

39
Q

what are 2 problematic side-effects of mirtazapine?

A

sedation and weight gain

40
Q

t/f MAO is involved in the metabolism of DA, NE and 5-HT both mentally and in the periphery

A

t

41
Q

t/f MAO shows no preference between DA, NE and 5-HT

A

true

42
Q

____ is a food source of monoamine that can have sympathomimetic effects

A

tyramine

43
Q

what are the sympathomimetic effects tyramine can have if MAO-A is inhibited?

A

hypertension and tachycardia

44
Q

what type of MAO is used to metabolize food sources of monoamines?

A

MAO-A

45
Q

what type of MAO has a preference for metabolizing DA?

A

MAO-B

46
Q

Phenelzine is a ____ (drug type)

A

non-selective MAOI

47
Q

does Phenelzine have a long or short duration of action? why?

A

long bc it binds irreversibly to the MAO enzyme

48
Q

t/f MAOIs have significant food and drug interactions

A

true

49
Q

what foods must be avoided when taking Phenelzine? what are the consequences?

A

food high tyramine such as beer, wine, aged cheese, smoked meat, other fermented/ pickled things; can cause life-threatening high blood pressure and tachycardia

50
Q

what are the 2 most common symptoms of anti-depressants?

A

GI upset and sexual disturbances

51
Q

do the GI symptoms of antidepressants persist or go away?

A

go away with time

52
Q

what causes the nausea and diarrhea associated with antidepressants?

A

too high levels of 5-HT in the gI tract

53
Q

do the sexual dysfunction symptoms of antidepressants persist or go away?

A

typically persist as long as taken

54
Q

what is the most common reason patients wish to discontinue their antidepressants?

A

sexual dysfunction side effects

55
Q

why are combinations of antidepressants not commonly used?

A

can result in addictive effects and serotonin syndrome

56
Q

what is serotonin syndrome?

A

life-threatening condition caused by too much serotonin receptor stimulation

57
Q

what is the scientific name for St. John’s wort?

A

hypericum perforatum

58
Q

what are the 2 active ingredients in St. John’s wort?

A

hypericin and hyperforin

59
Q

what is St. John’s wort?

A

natural health product used for many years as a “natural antidepressant”

60
Q

t/f st. johns wort has been seen to increase levels of DA, NE and 5-HT

A

true

61
Q

although clinical studies have shown that some preparations of st. johns wort are effective, what is something to consider with NHPs?

A

not all created by the same set of standard

62
Q

t/f st/johns wort has been found to be as effective as low dose TCA and SSRIs

A

t

63
Q

t/f st. johns wort has fewer side effects than TCAs

A

t

64
Q

st. Johns wort is a ___ inducer, resulting in interactions with many drugs

A

CTP

65
Q

what are some key drug classes St. John’s wort interacts with?

A

oral contraceptives, antihypertensives, antibiotics, anticoagulants, benzodiazepines

66
Q

is it dangerous to take st. johns wort with antidepressants?

A

yes! serotonin syndrome

67
Q

what are the symptoms of serotonin syndrome?

A

hypertension, tachycardia, tremor, muscle rigidity, rapid fluctuations in mental status, delirium, coma

68
Q

one theory for the need of 4-6 wks for a new antidepressant therapy to start working is that ____ is required to allow long-term changes in neuronal transmission

A

synaptic remodelling

69
Q

what needs time to be down regulated before that increased serotonin in the body can start to be effective when starting a new antidepressant?

A

autorecetptors

70
Q

how does the neurotrophic hypothesis play into the reason for antidepressants taking weeks to start working?

A

the continued enhancement of neuronal signalling brings changes in gene transcription that up-regulate BDNF production which promotes neurogenesis and remodelling of synapses for better transmission

.Pharmacology (55 decks)

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