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345A > Antidepressant notes > Flashcards

Antidepressant notes Flashcards

1
Q

T: Drugs used to treat mood disorders, OCD/eating disorders, chronic pain

A

antidepressants

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2
Q

4 things anti treat

A

Drugs used to treat mood disorders, OCD/eating disorders, chronic pain

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3
Q

2 ways antidepressants differ from stimulants

A
  1. Target brain, not parasympathetic system

2. Mechanism of action

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4
Q

antidepressants affect …. not … like stimulants

A

mood, arousal

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5
Q

what is the mechanism of action in antidepressants

A

second messenger/ mRNA factors

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6
Q

T: illness1 that affects how you feel, think and behave2 causing persistent feelings of sadness and loss of interest in previously enjoyed activities3.

A

major depressive disorder

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7
Q

illness1 that affects how you feel, think and behave2 causing persistent feelings of sadness and loss of interest in previously enjoyed activities3. explain what 1 implies

A

Biological origins

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8
Q

what are the biological origins of depression, what are the areas anatomically that we see differences in people with depression

A

anatomical differences have emerged in mesolimbic and frontal areas

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9
Q

antidepressants are only used to treat depression

A

f treat mood, OCD, eating and chronic pain disorders

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10
Q

what is the problem with the biological origins

A

correlation

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11
Q

antidepressants influence arousal

A

f do not change heart rate act, changes mood

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12
Q

do antidepressants target brain or body

A

brain(cognitive components)

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13
Q

illness1 that affects how you feel, think and behave2 causing persistent feelings of sadness and loss of interest in previously enjoyed activities3 explain 2

A

Holistic (not selective)

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14
Q

illness1 that affects how you feel, think and behave2 causing persistent feelings of sadness and loss of interest in previously enjoyed activities3 explain 3

A

not situational and comparative

comparing to times without depression e.g. if your pessimistic thats different

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15
Q

what is the common denominator of MDD

A

monamines

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16
Q

does stim influence the body or brain

A

body= working on NS= sympathomimetic

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17
Q

what monamines are influenced in MDD

A

seretonin
dopamine
nonep

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18
Q

seretonin influences what aspects of MDD

A

anxiety and obsession

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19
Q

nonep influences what aspects of MDD

A

alertness, attention, enjoyment

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20
Q

dopamine influences what aspects of MDD

A

motivation and reward

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21
Q

why and how does depression onset arise

A

permissive hypothesis

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22
Q

how was antidepressants found

A

TB treatment made people feel way better even though they still had symptoms

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23
Q

where did the permissive hypothesis come from

A

TB pills were seretonergics = improved mood
supposed that bcs of low serotonin in body system transforms dopamine into serotonin (body can do this easily) but as a result of compensation find stuff less rewarding and motivation that is naturally rewarding

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24
Q

T: low serotonin causes low norepinephrine/dopamine

A

permissive hypothesis

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25
Q

the permissive hypothesis says Dopamine compensates by providing more …

A

precursor

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26
Q

someone with OCD would have what monoamine imbalance

A

seretonin

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27
Q

what are the problems with permissive hypothesis 2

A
  • Intake is immediate, behavioural change is delayed

* general monoamine depletion doesn’t result in depression

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28
Q

it takes 2-4 weeks for antidepressants to work, why the delay

A

?

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29
Q

you can see depression from birth

A

f different onset than most other disorders

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30
Q

how can we best understand onset of depression

A

diathesis stress model (bio psyho social)

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31
Q

Diathesis stress support: emergence of depression in typical cohort who have experienced ….,

A

very stressful life events (kicks off depression)

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32
Q

Diathesis stress support: Family studies demonstrate … of depression

A

heritability

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33
Q

since dep is kicked off by stressful life event does that mean no genetic component

A

f just didn’t know what it meant

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34
Q

what is the heritability of depression

A

30-40%

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35
Q

why are heterability findings scewed 2

A

men vs female depression diagnosis

depressed mother deprives enviro

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36
Q

when does the cognitive aspect of MDD emerge

A

precede depression (thought processes before change in mood)

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37
Q

when do schemas (cognitive component) go away?

A

dissipate during remission of depression in response to stress

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38
Q

Organic stress, such as withdrawal, lack of sunlight (SADs), postpartum hormone, or drug abuse (DSM-5)* is known to induce depression

A

f depression like symptoms (comorbidity different from having disorder as result of)

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39
Q

what are the 3 types of antidepressants

A

first, second, third generation

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40
Q

what ae the 2 types of first generation

A

MAOIs and Trycylics

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41
Q

Inhibit enzyme which breaks down monoamines at synapse

A

MAOIs

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42
Q

what antidepressants inhibiting an inhibitor

A

MAOIs

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43
Q

what antidepressants causes the cheese reaction

A

MAOIs

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44
Q

the diagnosing of MDD requires a stressful life event

A

t

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45
Q

depression can happen to people with no family history

A

true

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46
Q

depression can happen to people with no family history

A

true

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47
Q

what’s the assumption of what caused depression in MAO time

A

too much of the MAO monoamine around which break apart and transform NT

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48
Q

what did they think MAOs

A

block off enzyme, so it won’t be breaking apart dopamine to create serotonin = enough serotonin in system

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49
Q

what were the problems with MAOIs

A

“cheese reaction”

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50
Q

what wasn’t being broken down that caused cheese reaction

A

tyramine

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51
Q

what does an increase in tyramine do to body

A

tyramine elevates blood pressure and results in stroke

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52
Q

T: Block reuptake of serotonin and norepinephrine at synapse

A

tricyclics

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53
Q

is the MAOI cheese reaction reversible?

A

no MAO inhibited for life

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54
Q

what was new about the new MAOIs

A

selectively block MAO A not MAO B = reversible MAOI after 20 y

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55
Q

what do the tycyclics selectively block

A

non. ep

dopamine and sert

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56
Q

problem with TCAs

A

produce irregular or elevated heart-rate

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57
Q

why were TCAs better than MAOIs

A

only change cognitive not physiological system

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58
Q

what about the TCAs produce irregular or elevated heart-rate

A

levo nonep has effects in body

59
Q

T: Selective Serotonin Reuptake inhibitors

A

second generation

60
Q

T: Serotonin-Norepinephrine Reuptake Inhibitors (SNRI)

A

third generation

61
Q

what were second gen antidepressants trying to avoid

A

attaching to nonep = heart problems

62
Q

what was the benefit of SSRIs

A

Reduced the cardiologic side-effects

63
Q

prozac is what kind of antidepressants

A

second gen

64
Q

was prozac discovered or designed

A

designed

65
Q

why did you not see heart problems in SNRIs even though the block nonep

A

targeted dex not levo nonep

66
Q

blocking reuptake of nonep might be dangerous as it resembles…

A

amphet= amphet psychosis

67
Q

what do third gen block

A

Block reuptake of both serotonin and norepinephrine in brain

68
Q

Are antidepressants effective?

A

no

69
Q

what was ineffective about 2nd and 3rd gen

A

did not understand secondary effects

70
Q

2nd /3rd gen. medication actively altered for depression use

A

t

71
Q

1st gen. anti-depressants “discovered” when treating other disorders what’s the problem with this

A

secondary effects, can’t understand what’s actually happening with disorder (mechanism)

72
Q

what happened when patent ran out

A

found out antisepsis were 50% effective

73
Q

how did placebo compare to second generation

A

??

74
Q

T: negative results found 50% of the time, however never promoted beyond FDA

A

Publication bias

75
Q

what NT represents mood and motivation in the system

A 
mood= seretonin 
motivation= dopamine
76
Q

why are people newly on antidepressants on suicide watch

A

increase in motivation takes on first before change in mood = serotonin. will to do stuff increases

77
Q

what protects people from suicdie in depression

A

no motivation= can’t leave bed

78
Q

when prozac was released to public there was a spike in suisides

A

t

79
Q

teenagers were just as likely to commit suicide on or off meds

A

t = no better option

80
Q

T: suicide warnings introduced in 2003 caused

a decrease in prescription to children/teens

A

black box

81
Q

what is primary effect of antidepressants

A

seretonin

82
Q

what is primary effect of antidepressants

A

seretonin

83
Q

3 other drugs that can treat depression

A

sympathomimetic stimulants
oxytocin
heterocyclic

84
Q

T: Amphetamine-like substances

A

Sympathomimetic Stimulants

85
Q

T: Hormone that rewards inter-personal behaviour

A

oxytoxin (give hormone that facilitates social bonding

86
Q

what’s the problem with treating depression with sympathomimetic stimulants

A

euphoria is an emotion whereas mood is a long term change = effects don’t last

87
Q

T: serious negative secondary/side effects: last resort

A

heterocyclic

88
Q

when you hug someone you get what NT

A

oxytocin

89
Q

do oxytocin medications work

A

in short term then gain tolerance

90
Q

different between tricyclics and heterocyclcis

A

?

91
Q

what systems do heterocyclic target

A

norep seretonin dopamine

92
Q

how do heterocyclic influence monamines

A

blocking reuptake and adding second kick of addictive effect

93
Q

3 mechanisms of action of Heterocyclics

A

Block reuptake of Norepinephrine and Serotonin

– Block dopamine transporter protein (reuptake mechanism) (?) – Stimulate release of Norepinephrine (?)

94
Q

what is the problem with heterocyclic

A

Block post-synaptic histamine, and acetylcholine receptors (hitting all quadrants makes everything more bioavalible)

95
Q

side effects (in body) of heterocyclic? 2

A

1) Sever cardiovascular irregularities

2) downregulation of Norepinephrine receptors

96
Q

any drug that plays with … system and you’ll have circulatory changes that effect the heart

A

norepinephrine changes

97
Q

the 2) downregulation of Norepinephrine receptors results in what kind of behaviour

A

resemble tolerance and withdrawal of amphetamines= reemergence of depressive symptoms

98
Q

how do heterocyclic result in reemergence of depressive symptoms

A

could be from tolerance form homeostatic or from rebound

99
Q

which antidepressants produces withdrawal symptoms

A

heterocyclic (mild)

100
Q

do you have drug seeking behaviour on antidepressants

A

f only heterocyclic

101
Q

what is the problem with withdrawal on heterocyclic

A

are behavioural or physiological?

102
Q

heterocyclic are More … than other antidepressants

A

toxic

103
Q

T: Delirium, seizures, light sensitivity, raised pulse rate, lowered core body temp, respiratory arrest, cardiovascular collapse, impaction (elderly)

A

toxic effects of other antidepressants

104
Q

4 problems of heterocyclic

A
  1. severe cardiovascular irregularities
  2. down regulation of nonep. receptors
  3. more toxic than other antidepressants
  4. more severe side effects
105
Q

the withdrawal symptoms of heterocyclic are the product of what problem with them

A

down regulation of nonep

106
Q

what are the side effects of heterocyclic

A

Anorexia, insomnia, anxiety, mania, psychotic episodes (amphet psychosis)

107
Q

T: the tendency for patients to suddenly (willingly) stop taking medication after four weeks, resulting in re- emergence of symptoms

A

discontinuation syndrome

108
Q

problems with discontinuation syndrome

A

unclear how discontinuation and symptoms interact don’t know why they go off them distance between how they feel and think

109
Q

how do patients describe the side effects of antidepressants (why they went off them)

A

side effects described as “brain shivers” or “brain numbing”

110
Q

when do patients report brain shivers

A

not when on meds only after

111
Q

is there consistency with which side-effects reported

A

f

112
Q

2 speculation of what may cause discontinuation syndrome

A

– patients feel better -> stop taking meds

– delayed/slow effects -> think it’s not working

113
Q

is discontinuation syndrome related to withdrawal

A

no rebound (can’t be because they would be wanting more of the drug)

114
Q

are the symptoms in patients who go off their antidepressants caused by tolerance

A

no

115
Q

do those who discontinue their meds move on to harder drugs = gateway?

A

no Patients do not exhibit drug-seeking behaviour just don’t want it anymore

116
Q

was the antidepressants causing compulsive, out of control, or negative
consequences?

A

no none

117
Q

why did patients go off meds then?

A

delayed response

118
Q

what sparked the debate of the mechanisms behind antidepressants?

A

late temporal onset to reward = feeling better

119
Q

is depression caused by serotonin imbalance

A

yes partly but brain cell growth and connections also play a role

120
Q

what area of the brain is smaller in depressed people

A

hippocampus and others

121
Q

what does the hippocampus control

A

memory and emotion (cells deteriorate)

122
Q

what happens when hippocampus neutrons are regenerated

A

mood improves

123
Q

why does serotonin improve mood then?

A

indirectly effect on cell growth (promote release of other chemicals that promote neurogenesis )

124
Q

what is the genetic component in depression

A

short or long serotonin gene (and others= different kinds of depression)

125
Q

what 2 systems os the hippocampus related to

A

limbic and cortical systems

126
Q

the hippocampus is very close to the …. which is in charge of +. and - emotions

A

amygdala

127
Q

does depression have a structural component

A

yes! synaptogenosis decrease (without this you’re in a rut)

128
Q

T: Both theories state that stress induces release of cortisol (hormone) that atrophies the hippocampus, resulting in MDD.

A

glucocorticoid or BDNF theory

129
Q

what does BDNF stand for

A

brain derived neurotropic factor

130
Q

T: chemical that facilitates growth

A

BDNF

131
Q

T: stage in cortisol development in which chemicals effect brain in a specific way

A

glucocorticoid

132
Q

which NT involved in fight or flight

A

nonep immediate system

cortisol longer term stress system

133
Q

T:induces cortisol release

A

Glucocorticoid

134
Q

problem with having too much Glucocorticoid in the system

A

shuts down aspects of system worried with anything other than worry

135
Q

what could be the treatment of too much glucocorticoid hormone

A

antagonizing glucocorticoid receptors

136
Q

T: facilitates neurogenesis (of the hippocampus)

A

BDNF

137
Q

problem with BDNF

A

too little of this chemical is produced

138
Q

treatment of too little of BDNF chemical produced

A

increase BDNF

139
Q

in response to same life stressors some people get depression some don’t why

A

BDNF allows bounce back (easier learning of coping strategies)

140
Q

which depression theory Best account for environmental influence on the emergence of depression

A

BDNF and gluco

141
Q

what would happen if increased BDNF

A

could have hyperconnectivity = disorder (need synaptic pruning

142
Q

what would happen if decreased glucocorticoid

A

don’t have natural stress response

143
Q

2 things “Glucocorticoid” or “BDNF” theory can account for that serotonin couldn’t

A

❑Best account for environmental influence on the emergence of depression
o May also help account for polyphony of depressions

345A (20 decks)

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