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345A > Antidepressants > Flashcards

Antidepressants Flashcards

1
Q

T: diminished or complete lack of interest in nor-mally pleasurable activities

A

anhedonia

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2
Q

what are the 3 key facets of symptoms of depression

A

affective, cognitive, and somatic symptoms

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3
Q

what are the sleep disturbances in depression

A

either in the form of difficulty falling and staying asleep or difficulty waking up and staying awake.

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4
Q

what is the psychomotor disturbance

A

either in the form of excessive motor activity and agitation or a significant lack of motor activity.

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5
Q

it is not depression if it stems from the loss of a loved one

A

f

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6
Q

less intense depression w same symptoms :T

A

persistent depressive disorder

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7
Q

major depressive dis-order is that it can occur in persons who do not actually feel depressed.

A

t may feel anhedonic but not sad

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8
Q

what are the different theories of depression

A

monoamine theory of depression

glucocorcirticoid theory of depression

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9
Q

what are the 3 monamines that relate to mood

A

dopamine, nonep and seretonin

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10
Q

all of the monoamine neurotransmit-ters have centers in the midbrain or upper brainstem and send projections forward to various parts of the limbic system and the forebrain through the ..

A

medial forebrain bundle

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11
Q

where do the NE, Da and 5 HT arise in the medial forebrain bundle

A

NE= locus coerulus
5 HT= raphe system
dopamine= VTA

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12
Q

T: depression is a result of reduced levels of activity in monoamine systems.

A

monoamine theory of depression

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13
Q

there is more depression in parkinsions patients why

A

depletion of dopamine

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14
Q

what about depression can’t be explained by the monoamine theory of depression 2

A
  • antidepressant medications pro-duce an immediate physiological effect but subjective depression alleviation takes awhile
  • correlation between tryptophan depletion and depression does not hold true for everyone
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15
Q

why does typtophan depletion effect

A

only those with history of depression in family

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16
Q

serotonin directly causes depression

A

f but plays a role in vulnerability to depression

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17
Q

individuals diag-nosed with major depressive disorder have low cerebrospi-nal-fluid levels of …, its amino acid precursor …, and its major metabolite … decreased numbers of 5-HT reuptake … in the brainstem

A

5-HT
tryptophan
5-H1AA.
trans-porter proteins (reduction in 5 HT)

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18
Q

is depression the result of a widespread dysregulation of serotonin

A
  • agent in control of the number of 5 HT transporter protein production has 2 forms long and short
  • differences in receptor binding
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19
Q

which gene makes of susceptible to depression

A

short

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20
Q

increases in serotonin receptor binding potential is suggested in depression

A

f some evidence suggests increases and some suggests decreases in 5-HT1A receptor binding potential in depres-sion.

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21
Q

5-HT1A receptors act not only as post-synaptic receptors, but also as …

A

autoreceptors.

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22
Q

stimulating 5 hT autorecetors does what to serotonin levels

A

lowers it by inhibiting cell firing (in Raf nuclei)

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23
Q

stimulating 5 HT receptors in the hippocampus, hypothalamus, amyg-dala, and cortex does what to serotonin levels

A

increase I t

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24
Q

Changes in the sensitivity or number of 5-HT1A receptors could be due to what 2 things

A

genes or adaptive compensatory response to depression

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25
Q

how important is serotonin in antidepression meds

A

nessasary but not sufficient for cure

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26
Q

why might adding serotonin with drug not lead to increased serotonin in brain for awhile?

A

takes a while for auto receptors to habituate (down regulate auto receptors)

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27
Q

what do antidepressants do to postsynaptic receptors

A

With chronic treatment, antidepres-sants are able to enhance the sensitivity and functioning of 5-HT1A postsynaptic receptors, leading to increased mono-amine activity

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28
Q

where does the 5-HT system in the brain run

A

from the raphe nuclei through the medial forebrain bundle to the forebrain

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29
Q

… activity is also dysregu-lated in depression

A

NE

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30
Q

what other NT could influence depression (not monoamine theory

A

GABA, acetylcholine, opioid peptides, and cannabinoids, and the balance achieved among levels of these neurotransmitters

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31
Q

T: an important part of the neuroendocrine system that controls the body’s response to stress.

A

HPA axis

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32
Q

what are the 5 stages of a stress response in HPA axis

A

CRH released in hypothalamus
ACTH from anterior pituitary
secretion of cortisol in adrenal glands

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33
Q

HPA axis is always active

A

f after stress in fight or flight ends it should stop through negative feedback to hypo to stop releasing CRH

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34
Q

in depression chronic-stress-induced overactivity of the HPA axis is due, at least in part, to a downregulation of glucocorticoid receptors in the hip-pocampus :T

A

glucocorticoid theory of depression

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35
Q

neurons that contain CRH are in what parts of brain

A

hypo and limbic system (mood)

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36
Q

what are the limbic areas 7

A

amygdala, hippocampus, thalamus, hypothalamus, basal ganglia, and cingulate gyrus

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37
Q

A very common finding in patients with depression is structural change in areas of the limbic sys-tem

A

t

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38
Q

The hypothalamic–pituitary–adrenal axis image on p. 295

A

review

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39
Q

what brain areas looses volume in depression

A

prefrontal and hippocampus

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40
Q

what increases volume with depression

A

Amygdala

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41
Q

Because the prefrontal cortex, hippocampus, and
amygdala are interconnected with the hypothalamus, struc-tural changes in these brain regions lead to a loss of balance between inhibition and excitation of the stress system, = …….

A

heightened stress hormone release

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42
Q

therapeutic potential of CRH receptor antagonists?

A

mixed It may be that CRH antagonists benefit only those individuals whose depres-sion is brought on by stress and resulting hyperactivity of the HPA axis

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43
Q

how are these 2 theories of depression related

A

stress hormoones interact with monoamine systems

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44
Q

how does cortisol influence monoamine systems

A

more Da release= up regulation of dopamine receptors in VTA

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45
Q

T: anti reward system

A

stress sytem

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46
Q

what accounts for the depressive anxious symptoms of withdrawal

A

sensitization fo the stress system leads to depressive symptoms

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47
Q

During stressful events, .. activity overrides that of the prefrontal cortex and activates stress pathways in the …2, leading to increased lev-els of monoamines and perhaps even upregulation of their receptors

A

amygdala
hypothalamus and brainstem (change in the structure or activity of the amygdala has the potential to produce changes in the functioning of monoamine systems)

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48
Q

Changes in glucocorticoid levels are also strongly associated with changes in 5-HT function

A

stress and reduction of 5HT in the hippocampus

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49
Q

(the surgical removal of the adrenal glands, thereby clearing the body of cortisol does what to 5 HT

A

increases receptor densities and binding

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50
Q

if 5 HT levels are changed by stressful life events is there any genetic component

A

certain individuals are genetically predisposed to develop HPA-axis hyperactivity (short 5 HT

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51
Q

what does early stressful experiences do to HPA response later in life

A

primes it to overreact

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52
Q

Antidepressant medications reduce HPA-axis activity by increasing the number of … receptors to create more efficient negative-feedback loops

A

cortisol

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53
Q

nor-malizing the stress response may be a necessary condition in order for antidepressants to work

A

t

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54
Q

what are the 2 first ten antidepressants

A

MAOIs and tricyclic antidepressants

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55
Q

the first MAOI was first a … treatment

A

TB

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56
Q

are MAOIs still effective in treating depression

A

yes

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57
Q

how do the tricyclics get their name

A

r molecular structure contains three rings of atoms

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58
Q

why did MAOIs loose popularity for awhile

A

liver damage on too high doses

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59
Q

what were the second generation antidepressants

A

SSRIs

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60
Q

most well known SSRI

A

prozac (similar structure to tricyclics but less side effects also treated anxiety)

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61
Q

other name for third gen antidepressants

A

atypical SNRIs

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62
Q

the stimulation of the rhiticular formation NE activity helps what depression symptoms

A

fatigue and loss of energy

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63
Q

3 main drug classes of antidepressants

A

MAOIs
trycyclics
SSRIs

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64
Q

what does SNDRIs stand for

A

Triple monoamine reuptake inhibitors, also known as sero-tonin-norepinephrine-dopamine reuptake inhibitors

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65
Q

how do the different antidepressants classes differ in absorption

A

similar

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66
Q

put in order of faster to slowest absorption

A

TCAs

SSRIs and SNRIs

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67
Q

Antidepressants generally have low levels of protein binding

A

f high

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68
Q

TCAs: first pass metabolism is inhibited by alcohol what does this do to antidepressants

A

more absorption (doesn’t happen for SSR and NIs)

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69
Q

SSRis should not be combined with alcohol

A

f can be used to treat it

70
Q

how easily do antidepressants cross the blood brain barrier

A

readily

71
Q

where do antidepressants get concentrated in distribution 4

A

lungs, kidneys, liver, and brain

72
Q

how do the half lives of the antidepressants compare

A

MAOIs short 2-4 hours
second and third gen
TACs 24 hours

73
Q

how do half lives influence how often you have to take dose of antidepressants

A

13.4.3 elimination ??

74
Q

do SSRIs have active metabolites

A

no

75
Q

how do inidivudals differ in the pharmacokinetics of antidepressants

A

some people don’t have emzymes to destroy drugs = extremely long half lives, can build to toxic level
ethnicity influence enzymes

76
Q

why the lag between antidepressants admin and alleviation of symptoms

A

neuroadaptations that must take place (specifi-cally, the downregulation of 5-HT1A autoreceptors and increase in serotonin system function

77
Q

All monoamine neurons produce the enzyme …

A

monoamine oxidase (MAO)

78
Q

what does monoamine oxidase (MAO) do

A

degrades monoamine mole-cules that float freely (i.e., those that are outside of vesicles) in the cytosol of the axon terminal, thereby diminishing available neurotransmitter

79
Q

so what do MAOIs do

A

block monoamine oxidase (MAO)to up monoamine levels (increase the availability and activity of DA, NE, and 5-HT)

80
Q

what are the 2 types of MAO

A

MAO A

MAOB

81
Q

What does MAOA do

A

degrades all three monoamines

82
Q

what does MAO B do

A

most active in metabolizing DA

83
Q

why did the unselective MAOIs produce unpleasant side effects

A

Because both forms of MAO enzymes are present throughout the body`

84
Q

what do newer MAOIs selectively act on

A

MAO-B at low doses but, at higher doses, also affect MAO-A

85
Q

T: they can detach from MAO rather than deac-tivate it permanently.

A

reversible

86
Q

Trycylics act similarly to MAOis as first gen

A

f more like SSRIs

87
Q

what is the mechanism of action for tricyclics

A

block reuptake transporter proteins on the axon terminals of 5-HT and NE neurons

88
Q

do all tricyclics act the same

A

no various effects

89
Q

do tricyclics have side effects

A

additional actions mean they have unpleasant sometimes dangerous side effects

90
Q

the SSRIs effect all monomies just 5 HT more

A

f

91
Q

can SSRIs select which 5 HT receptor to bind to

A

SSRIs are not selective with regard to the subtype of serotonin receptor to which they bind

92
Q

. It is believed that the antidepressant effects of the SSRIs result from altera-tions to … functioning whereas the unpleas-ant side effects of the SSRIs may be due to activation of …

A

5-HT1A receptor

5-HT2 receptors.

93
Q

bupropion is which types of antidepressants

A

atypical

94
Q

RIs and atypicals do what to 5HT, dopamine and nonep

A

block the reuptake of 5-HT, NE, and in some cases DA

95
Q

what’s another way ayticals may work

A

act by antagonizing autoreceptors, specifically for NE and 5-HT, to prevent inhibitory feed-back to the cell and thereby increase the amount of trans-mitter released

96
Q

how is the effect of blocking histamine receptors

A

induce sedation and drowsiness = treats insomnia component of depression

97
Q

side effects of MAOIs

A

tremors, weight gain, blurry vision, dry mouth, low blood pressure

98
Q

T: MAOI side effect dizziness or fainting when moving to a standing position after being seated or lying down

A

postural hypertension

99
Q

when are MAOIs dangerous

A

with other drugs or foods

100
Q

MAOIs can increase the power of MDMA and cocaine (monoamine-stimulating drugs) why these drugs

A

they rely on the enzymes that MAOIs block

101
Q

MAOIs also potentiate the … effects of heroin

A

hypotensive and CNS-depressant

102
Q

T: danger of antidep
cognitive symptoms, including disorientation, confusion, and agitation. Somatic symptoms, some of which can be life-threatening, reflect the dysregulation of autonomic nervous system functioning

A

seretonin syndrome

103
Q

what are the symptoms of serotonin syndrome

A

rapid and irregular heartbeat, pupil dilation, flushing, shivering, sweating, and diarrhea. Severe headache, a loss of motor coordina-tion, shock, seizures, and unconsciousness are also possi-ble

104
Q

what causes serotonin syndrome

A

acute dramatic increases in serotonin transmutation

105
Q

seretonin syndrome can occur from a switch in medica-tions can lead if there is an insuffi-cient … time—the period required for a drug to be completely eliminated from the body

A

washout (more common when switching from antidepressants with long half life)

106
Q

substance found in food that relies on monoamine oxidase

A

tyramine

107
Q

what foods is tyramine in

A

aged hard cheeses; pickled, aged, smoked, or processed meats including fish, poultry, beef, and pork; some beans, peas, fruits, vegetables, and nuts; beer, wine, and other alcoholic beverages; some energy drinks; and chocolate.

108
Q

what happens if you eat tyramine rich foods while on MAOIs

A

it doesn’t break down and accumulates

109
Q

tyramine when not Brocken down crosses the blood brain barrier influencing CNS

A

f it is capable of stimulating the release of catechol-amines (NE and E) in the peripheral nervous system

110
Q

T: are hormones made by your adrenal glands, which are located on top of your kidneys sent into blood when stressed

A

catecholamines

111
Q

what are the behavioural effects of tyramine build up

A

causes effects that mimic sympathetic nervous system acti-vation, including sweating, nausea, and increased blood pressure, which in turn can produce headaches, internal bleeding, and even stroke or death

112
Q

T: causes effects that mimic sympathetic nervous system acti-vation, including sweating, nausea, and increased blood pressure, which in turn can produce headaches, internal bleeding, and even stroke or death

A

cheese effect

113
Q

is selectively avoiding the MAO B enough to let you digest tyramine

A

yes tyramine that gets past the inhibited MAO-A in the intestine can still be metabolized by the MAO-B in the liver and lungs (selective safer)

114
Q

when is the best time to take MAOIs in comparison to eating

A

long after eating so tyramine can be metabolized

115
Q

The tricyclics also affect autonomic nervous system functioning through their …

A

anticholinergic effects

116
Q

agent is a substance that blocks the action of the neurotransmitter acetylcholine at synapses in the central and the peripheral nervous system:T

A

anticholinergic

117
Q

TCAs inhibit the … division of the autonomic nervous system, which uses ACh as a trans-mitter.

A

parasympathetic

118
Q

what are the effects of TCAs parasympathetic inhibition

A

dry mouth, constipation, blurred vision, ringing in the ears, and urine retention, excessive sweating, weight gain .

119
Q

Parkinsonian symptoms are similar to

the side effects of …

A

antipsychotics

120
Q

why do TCAs cause weight gain

A

This may be due to the influence of TCAs on hista-mine activity

121
Q

side effect of which antidepressants: reduction in seizure threshold, which can cause convulsions, especially in those with pre-existing seizure disorders

A

TCA

122
Q

which antidepressants has least side effects and why

A

The SSRIs have fewer nonspecific actions on systems

outside of serotonin

123
Q

side effects of SSRIs

A

intestine problems, headaches, dizziness, sweating, nervousness, and agitation, but these symptoms tend to dissipate with time.

124
Q

what do SSRIs do to appetite

A

decrease it

125
Q

what causes the side effects from third gen medications

A

due to this class’s antagonism of acetylcholine and histamine receptors and enhancement of 5-HT2–3
receptor activity

126
Q

what are the side effects of third gen

A

increased appetite and weight gain, changes in blood pres-sure, dizziness, dry mouth, and gastrointestinal problems.

127
Q

what 3rd gen antidepressants increases the risk for seizure

A

bupropin

128
Q

which class of antidepressants is most effective

A

roughly the same for all but individual differences

129
Q

which antidepressants would you use if you also had anxiety

A

SSRI or SNRI

130
Q

why are there so many antidepressants available

A

side effects differ for people

131
Q

why : SSRIs are far superior to any other antidepressants in terms of patients’ remaining compliant to chronic drug regimens

A

low unwanted side effects

132
Q

mere expectation of improvement can account for up to ..% of the improvement that actu-ally occurs

A

75

133
Q

why is the placebo effect growing

A

expectancy effects due to increased belief that they work

134
Q

in patients experiencing mild or moderate depression, placebos and antidepressants are equally effective in alleviating symptoms

A

t

135
Q

in the most extreme cases of depression antidepressants are more effective

A

is due to a decreased effectiveness of the placebo rather than an increased effectiveness of the anti-depressant

136
Q

for adolescence which antidepressants work

A

SSRI

137
Q

what are some of the side effects adolescence experience in response to SSRIs

A

agitation, hyperactivity, and symptoms of mania

138
Q

antidepressants are reinforcing due to pleasant effects experienced

A

f not self administers

139
Q

the antidepressants that work on dopamine produce euphoria

A

f low increases achieved slowly

140
Q

fluoxetine and other SSRIs
are useful in treating people with diagnosed personality disorders, such as obsessive-compulsive personality disor-der, and with compulsive behaviors: does it chqange personality then?

A

debate

141
Q

which antidepressants effect sleep

A

all

142
Q

what do the MAOIs do the sleep

A

cause either insomnia or sedation.

143
Q

what do the trycyclics do the sleep

A

driowsiness (from anticholinergic properties of drug) used treat insomnia but doesn’t increase total sleep time

144
Q

effects of fluoxetine and venlaxafine on sleep?

A

reduce REM= improve depression

145
Q

why do third gen cause sedation and sleepiness

A

have antihista-minergic actions and cause sedation and sleepiness, while others, like bupropion, can produce insomnia.

146
Q

why do third gen cause sedation and sleepiness

A

have antihista-minergic actions and cause sedation and sleepiness, while others, like bupropion, can produce insomnia.

147
Q

how do TCAs influence performance

A

imipramine and amitriptyline appear to exert detrimental effects on the performance of vigilance tasks and can cause cognitive, memory, and psychomotor impairments that seem to be related to the sedating effects of the drug

148
Q

how did SNRIs and SSRIs compare in working memory performance

A

both improved SNRIs more

149
Q

how do MAOIs influence performance

A

impairs psychomotor performance

150
Q

TACs and SSRIs cause impaired driving

A

more collisions t

151
Q

can you develop tolerance to antidepressants? to their side effects?

A

debate

after several weeks tolerate side effects except for fatigue with SSRIs

152
Q

do TCAs give you withdrawal? what is it like?

A

at high doses

restlessness, anxiety, chills, akathisia, and muscle aches

153
Q

do SSRIs give you withdrawal? what is it like?

A

dizziness, light-headedness, insomnia, fatigue, anxiety, nausea, headache, and sensory disturbances

154
Q

do SNRIs give you withdrawal? what is it like?

A

can be serious and include both bodily symptoms, such as heart palpitations and nausea, and psychiatric symptoms including delusions.

155
Q

what are the harmful effects of antidepressants

A

reproduction

156
Q

how do antidepressants influence sexual functioning

A

difficulty achieving orgasm

157
Q

the difficulty achieving orgasm is caused by sedation and fatigue

A

f

158
Q

which antidepressants is not associated with sexual dysfunction and why

A

bupropion does not effect 5 HT may even enhance due to dopamine

159
Q

how do antidepressants influence the fetus

A

some SSRIs and TCA increased risk of major fetal malformation, particularly cardiac defects, and newborn persistent pulmonary hypertension
atypical don’t show risks to fetus

160
Q

fluoxetine, a SSRI is correlated with intense, violent suicidal preoccupations in some patients

A

t

161
Q

without antidepressants people were twice as likely as those taking placebos to have sui-cidal ideations and to attempt suicide

A

f those taking antidepressant medications twice as likely (in young adults mostly)

162
Q

fluoxetine may induce an activating effect marked by racing thoughts, nervousness, and tremor what kind of antidepressants

A

SSRI

163
Q

T: a move-ment disorder characterized by restlessness, agitation, an inability to sit still, and a compulsion to be continuously active.

A

akathisia (associated with fluoxetine)

164
Q

can you overdose on antidepressants

A

second and third gen safer = rare to overdose but can be dangerous though serotonin syndrome

165
Q

dangers of TCAs?

A

toxic due to their their effect on the contractility of the heart muscle

166
Q

what are treatments for depression other than antidepressants

A

St johns wart
herbal treatments
light therapy, yoga, acupuncture, mindfulness-based therapy, and sleep-deprivation

167
Q

how effective is ECT

A

result in neurogenesis counteract cell death caused by cortisol

168
Q

high circulating levels of cortisol and may, in turn, facilitate hyperactivity of the …stress response in a sort of perpetually damaging feedback loop.

A

HPA-axis

169
Q

ECT increases BDNF levels and neurogene-sis in these regions, as do antidepressant drugs what is BDNF

A

protein: brain derived neurotopic factor (BDNF)

170
Q

other brain stimulating methods of treating? 2

A

transcranial magnetic stimulation and Deep brain stim

171
Q

exercise treats depression, how 2

A

promotion of hippocampal neurogene-sis, increases in 5-HT and BDNF levels, and a decrease in HPA-axis activity and cortisol production

172
Q

normalization of amygdala activity, and improved PFC–limbic connectivity, Serotonin trans-porter protein levels also show normalization after a year of …

A

psychodynamic therapy

345A (20 decks)

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