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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
fluoxetine MOA:
selectively blocks SERT so only 5-HT levels increase in the synapse
26
what class of drug is fluoxetine?
SSRI
27
does fluoxetine have any impact on NE?
no
28
SNRIs and TCAs target both ___ and ___
SERT and NET
29
SNRIs and TCAs reduce the re-uptake of both ___ and __
serotonin and NE
30
Venlafaxine is a ____(drug class)
SNRIs
31
which has fewer off-target effects, SNRIs or TCAs?
SNRIs
32
most of the side effects that occur with SNRIs are related to
elevated NE and 5-HT levels
33
amitriptyline is a ____ (drug Class)
TCA
34
why are there more side effects associated with TCAs?
they have significant binding to other receptors
35
what are 3 off-target receptors that TCAs bind to?
muscarinic; alpha 1 adrenergic, H1
36
what type of auto receptors are booked by mirtazapine?
alpha 2
37
when auto receptors are activated a ___coupled signalling cascade occurs, which ____(increases/decreases) the NT releases
Gi; decreases
38
what is an off-target receptor that mirtzapine binds strongly to?
H1 (blocks histamine)
39
what are 2 problematic side-effects of mirtazapine?
sedation and weight gain
40
t/f MAO is involved in the metabolism of DA, NE and 5-HT both mentally and in the periphery
t
41
t/f MAO shows no preference between DA, NE and 5-HT
true
42
____ is a food source of monoamine that can have sympathomimetic effects
tyramine
43
what are the sympathomimetic effects tyramine can have if MAO-A is inhibited?
hypertension and tachycardia
44
what type of MAO is used to metabolize food sources of monoamines?
MAO-A
45
what type of MAO has a preference for metabolizing DA?
MAO-B
46
Phenelzine is a ____ (drug type)
non-selective MAOI
47
does Phenelzine have a long or short duration of action? why?
long bc it binds irreversibly to the MAO enzyme
48
t/f MAOIs have significant food and drug interactions
true
49
what foods must be avoided when taking Phenelzine? what are the consequences?
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
what are the 2 most common symptoms of anti-depressants?
GI upset and sexual disturbances
51
do the GI symptoms of antidepressants persist or go away?
go away with time
52
what causes the nausea and diarrhea associated with antidepressants?
too high levels of 5-HT in the gI tract
53
do the sexual dysfunction symptoms of antidepressants persist or go away?
typically persist as long as taken
54
what is the most common reason patients wish to discontinue their antidepressants?
sexual dysfunction side effects
55
why are combinations of antidepressants not commonly used?
can result in addictive effects and serotonin syndrome
56
what is serotonin syndrome?
life-threatening condition caused by too much serotonin receptor stimulation
57
what is the scientific name for St. John's wort?
hypericum perforatum
58
what are the 2 active ingredients in St. John's wort?
hypericin and hyperforin
59
what is St. John's wort?
natural health product used for many years as a "natural antidepressant"
60
t/f st. johns wort has been seen to increase levels of DA, NE and 5-HT
true
61
although clinical studies have shown that some preparations of st. johns wort are effective, what is something to consider with NHPs?
not all created by the same set of standard
62
t/f st/johns wort has been found to be as effective as low dose TCA and SSRIs
t
63
t/f st. johns wort has fewer side effects than TCAs
t
64
st. Johns wort is a ___ inducer, resulting in interactions with many drugs
CTP
65
what are some key drug classes St. John's wort interacts with?
oral contraceptives, antihypertensives, antibiotics, anticoagulants, benzodiazepines
66
is it dangerous to take st. johns wort with antidepressants?
yes! serotonin syndrome
67
what are the symptoms of serotonin syndrome?
hypertension, tachycardia, tremor, muscle rigidity, rapid fluctuations in mental status, delirium, coma
68
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
synaptic remodelling
69
what needs time to be down regulated before that increased serotonin in the body can start to be effective when starting a new antidepressant?
autorecetptors
70
how does the neurotrophic hypothesis play into the reason for antidepressants taking weeks to start working?
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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