Antidepressant notes Flashcards
1
Q
T: Drugs used to treat mood disorders, OCD/eating disorders, chronic pain
A
antidepressants
2
Q
4 things anti treat
A
Drugs used to treat mood disorders, OCD/eating disorders, chronic pain
3
Q
2 ways antidepressants differ from stimulants
A
- Target brain, not parasympathetic system
2. Mechanism of action
4
Q
antidepressants affect …. not … like stimulants
A
mood, arousal
5
Q
what is the mechanism of action in antidepressants
A
second messenger/ mRNA factors
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
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
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
9
Q
antidepressants are only used to treat depression
A
f treat mood, OCD, eating and chronic pain disorders
10
Q
what is the problem with the biological origins
A
correlation
11
Q
antidepressants influence arousal
A
f do not change heart rate act, changes mood
12
Q
do antidepressants target brain or body
A
brain(cognitive components)
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)
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
15
Q
what is the common denominator of MDD
A
monamines
16
Q
does stim influence the body or brain
A
body= working on NS= sympathomimetic
17
Q
what monamines are influenced in MDD
A
seretonin
dopamine
nonep
18
Q
seretonin influences what aspects of MDD
A
anxiety and obsession
19
Q
nonep influences what aspects of MDD
A
alertness, attention, enjoyment
20
Q
dopamine influences what aspects of MDD
A
motivation and reward
21
Q
why and how does depression onset arise
A
permissive hypothesis
22
Q
how was antidepressants found
A
TB treatment made people feel way better even though they still had symptoms
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
24
Q
T: low serotonin causes low norepinephrine/dopamine
A
permissive hypothesis
25
the permissive hypothesis says Dopamine compensates by providing more ...
precursor
26
someone with OCD would have what monoamine imbalance
seretonin
27
what are the problems with permissive hypothesis 2
* Intake is immediate, behavioural change is delayed
| * general monoamine depletion doesn’t result in depression
28
it takes 2-4 weeks for antidepressants to work, why the delay
?
29
you can see depression from birth
f different onset than most other disorders
30
how can we best understand onset of depression
diathesis stress model (bio psyho social)
31
Diathesis stress support: emergence of depression in typical cohort who have experienced ....,
very stressful life events (kicks off depression)
32
Diathesis stress support: Family studies demonstrate ... of depression
heritability
33
since dep is kicked off by stressful life event does that mean no genetic component
f just didn't know what it meant
34
what is the heritability of depression
30-40%
35
why are heterability findings scewed 2
men vs female depression diagnosis
| depressed mother deprives enviro
36
when does the cognitive aspect of MDD emerge
precede depression (thought processes before change in mood)
37
when do schemas (cognitive component) go away?
dissipate during remission of depression in response to stress
38
Organic stress, such as withdrawal, lack of sunlight (SADs), postpartum hormone, or drug abuse (DSM-5)* is known to induce depression
f depression like symptoms (comorbidity different from having disorder as result of)
39
what are the 3 types of antidepressants
first, second, third generation
40
what ae the 2 types of first generation
MAOIs and Trycylics
41
Inhibit enzyme which breaks down monoamines at synapse
MAOIs
42
what antidepressants inhibiting an inhibitor
MAOIs
43
what antidepressants causes the cheese reaction
MAOIs
44
the diagnosing of MDD requires a stressful life event
t
45
depression can happen to people with no family history
true
46
depression can happen to people with no family history
true
47
what's the assumption of what caused depression in MAO time
too much of the MAO monoamine around which break apart and transform NT
48
what did they think MAOs
block off enzyme, so it won't be breaking apart dopamine to create serotonin = enough serotonin in system
49
what were the problems with MAOIs
“cheese reaction”
50
what wasn't being broken down that caused cheese reaction
tyramine
51
what does an increase in tyramine do to body
tyramine elevates blood pressure and results in stroke
52
T: Block reuptake of serotonin and norepinephrine at synapse
tricyclics
53
is the MAOI cheese reaction reversible?
no MAO inhibited for life
54
what was new about the new MAOIs
selectively block MAO A not MAO B = reversible MAOI after 20 y
55
what do the tycyclics selectively block
non. ep
| dopamine and sert
56
problem with TCAs
produce irregular or elevated heart-rate
57
why were TCAs better than MAOIs
only change cognitive not physiological system
58
what about the TCAs produce irregular or elevated heart-rate
levo nonep has effects in body
59
T: Selective Serotonin Reuptake inhibitors
second generation
60
T: Serotonin-Norepinephrine Reuptake Inhibitors (SNRI)
third generation
61
what were second gen antidepressants trying to avoid
attaching to nonep = heart problems
62
what was the benefit of SSRIs
Reduced the cardiologic side-effects
63
prozac is what kind of antidepressants
second gen
64
was prozac discovered or designed
designed
65
why did you not see heart problems in SNRIs even though the block nonep
targeted dex not levo nonep
66
blocking reuptake of nonep might be dangerous as it resembles...
amphet= amphet psychosis
67
what do third gen block
Block reuptake of both serotonin and norepinephrine in brain
68
Are antidepressants effective?
no
69
what was ineffective about 2nd and 3rd gen
did not understand secondary effects
70
2nd /3rd gen. medication actively altered for depression use
t
71
1st gen. anti-depressants “discovered” when treating other disorders what's the problem with this
secondary effects, can't understand what's actually happening with disorder (mechanism)
72
what happened when patent ran out
found out antisepsis were 50% effective
73
how did placebo compare to second generation
??
74
T: negative results found 50% of the time, however never promoted beyond FDA
Publication bias
75
what NT represents mood and motivation in the system
```
mood= seretonin
motivation= dopamine
```
76
why are people newly on antidepressants on suicide watch
increase in motivation takes on first before change in mood = serotonin. will to do stuff increases
77
what protects people from suicdie in depression
no motivation= can't leave bed
78
when prozac was released to public there was a spike in suisides
t
79
teenagers were just as likely to commit suicide on or off meds
t = no better option
80
T: suicide warnings introduced in 2003 caused
| a decrease in prescription to children/teens
black box
81
what is primary effect of antidepressants
seretonin
82
what is primary effect of antidepressants
seretonin
83
3 other drugs that can treat depression
sympathomimetic stimulants
oxytocin
heterocyclic
84
T: Amphetamine-like substances
Sympathomimetic Stimulants
85
T: Hormone that rewards inter-personal behaviour
oxytoxin (give hormone that facilitates social bonding
86
what's the problem with treating depression with sympathomimetic stimulants
euphoria is an emotion whereas mood is a long term change = effects don't last
87
T: serious negative secondary/side effects: last resort
heterocyclic
88
when you hug someone you get what NT
oxytocin
89
do oxytocin medications work
in short term then gain tolerance
90
different between tricyclics and heterocyclcis
?
91
what systems do heterocyclic target
norep seretonin dopamine
92
how do heterocyclic influence monamines
blocking reuptake and adding second kick of addictive effect
93
3 mechanisms of action of Heterocyclics
Block reuptake of Norepinephrine and Serotonin
| – Block dopamine transporter protein (reuptake mechanism) (?) – Stimulate release of Norepinephrine (?)
94
what is the problem with heterocyclic
Block post-synaptic histamine, and acetylcholine receptors (hitting all quadrants makes everything more bioavalible)
95
side effects (in body) of heterocyclic? 2
1) Sever cardiovascular irregularities
| 2) downregulation of Norepinephrine receptors
96
any drug that plays with ... system and you'll have circulatory changes that effect the heart
norepinephrine changes
97
the 2) downregulation of Norepinephrine receptors results in what kind of behaviour
resemble tolerance and withdrawal of amphetamines= reemergence of depressive symptoms
98
how do heterocyclic result in reemergence of depressive symptoms
could be from tolerance form homeostatic or from rebound
99
which antidepressants produces withdrawal symptoms
heterocyclic (mild)
100
do you have drug seeking behaviour on antidepressants
f only heterocyclic
101
what is the problem with withdrawal on heterocyclic
are behavioural or physiological?
102
heterocyclic are More ... than other antidepressants
toxic
103
T: Delirium, seizures, light sensitivity, raised pulse rate, lowered core body temp, respiratory arrest, cardiovascular collapse, impaction (elderly)
toxic effects of other antidepressants
104
4 problems of heterocyclic
1. severe cardiovascular irregularities
2. down regulation of nonep. receptors
3. more toxic than other antidepressants
4. more severe side effects
105
the withdrawal symptoms of heterocyclic are the product of what problem with them
down regulation of nonep
106
what are the side effects of heterocyclic
Anorexia, insomnia, anxiety, mania, psychotic episodes (amphet psychosis)
107
T: the tendency for patients to suddenly (willingly) stop taking medication after four weeks, resulting in re- emergence of symptoms
discontinuation syndrome
108
problems with discontinuation syndrome
unclear how discontinuation and symptoms interact don't know why they go off them distance between how they feel and think
109
how do patients describe the side effects of antidepressants (why they went off them)
side effects described as “brain shivers” or “brain numbing”
110
when do patients report brain shivers
not when on meds only after
111
is there consistency with which side-effects reported
f
112
2 speculation of what may cause discontinuation syndrome
– patients feel better -> stop taking meds
| – delayed/slow effects -> think it’s not working
113
is discontinuation syndrome related to withdrawal
no rebound (can't be because they would be wanting more of the drug)
114
are the symptoms in patients who go off their antidepressants caused by tolerance
no
115
do those who discontinue their meds move on to harder drugs = gateway?
no Patients do not exhibit drug-seeking behaviour just don't want it anymore
116
was the antidepressants causing compulsive, out of control, or negative
consequences?
no none
117
why did patients go off meds then?
delayed response
118
what sparked the debate of the mechanisms behind antidepressants?
late temporal onset to reward = feeling better
119
is depression caused by serotonin imbalance
yes partly but brain cell growth and connections also play a role
120
what area of the brain is smaller in depressed people
hippocampus and others
121
what does the hippocampus control
memory and emotion (cells deteriorate)
122
what happens when hippocampus neutrons are regenerated
mood improves
123
why does serotonin improve mood then?
indirectly effect on cell growth (promote release of other chemicals that promote neurogenesis )
124
what is the genetic component in depression
short or long serotonin gene (and others= different kinds of depression)
125
what 2 systems os the hippocampus related to
limbic and cortical systems
126
the hippocampus is very close to the .... which is in charge of +. and - emotions
amygdala
127
does depression have a structural component
yes! synaptogenosis decrease (without this you're in a rut)
128
T: Both theories state that stress induces release of cortisol (hormone) that atrophies the hippocampus, resulting in MDD.
glucocorticoid or BDNF theory
129
what does BDNF stand for
brain derived neurotropic factor
130
T: chemical that facilitates growth
BDNF
131
T: stage in cortisol development in which chemicals effect brain in a specific way
glucocorticoid
132
which NT involved in fight or flight
nonep immediate system
| cortisol longer term stress system
133
T:induces cortisol release
Glucocorticoid
134
problem with having too much Glucocorticoid in the system
shuts down aspects of system worried with anything other than worry
135
what could be the treatment of too much glucocorticoid hormone
antagonizing glucocorticoid receptors
136
T: facilitates neurogenesis (of the hippocampus)
BDNF
137
problem with BDNF
too little of this chemical is produced
138
treatment of too little of BDNF chemical produced
increase BDNF
139
in response to same life stressors some people get depression some don't why
BDNF allows bounce back (easier learning of coping strategies)
140
which depression theory Best account for environmental influence on the emergence of depression
BDNF and gluco
141
what would happen if increased BDNF
could have hyperconnectivity = disorder (need synaptic pruning
142
what would happen if decreased glucocorticoid
don't have natural stress response
143
2 things “Glucocorticoid” or “BDNF” theory can account for that serotonin couldn't
❑Best account for environmental influence on the emergence of depression
o May also help account for polyphony of depressions
