Antidepressants Flashcards
1
Q
T: diminished or complete lack of interest in nor-mally pleasurable activities
A
anhedonia
2
Q
what are the 3 key facets of symptoms of depression
A
affective, cognitive, and somatic symptoms
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.
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.
5
Q
it is not depression if it stems from the loss of a loved one
A
f
6
Q
less intense depression w same symptoms :T
A
persistent depressive disorder
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
8
Q
what are the different theories of depression
A
monoamine theory of depression
glucocorcirticoid theory of depression
9
Q
what are the 3 monamines that relate to mood
A
dopamine, nonep and seretonin
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
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
12
Q
T: depression is a result of reduced levels of activity in monoamine systems.
A
monoamine theory of depression
13
Q
there is more depression in parkinsions patients why
A
depletion of dopamine
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
15
Q
why does typtophan depletion effect
A
only those with history of depression in family
16
Q
serotonin directly causes depression
A
f but plays a role in vulnerability to depression
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)
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
19
Q
which gene makes of susceptible to depression
A
short
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.
21
Q
5-HT1A receptors act not only as post-synaptic receptors, but also as …
A
autoreceptors.
22
Q
stimulating 5 hT autorecetors does what to serotonin levels
A
lowers it by inhibiting cell firing (in Raf nuclei)
23
Q
stimulating 5 HT receptors in the hippocampus, hypothalamus, amyg-dala, and cortex does what to serotonin levels
A
increase I t
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
25
how important is serotonin in antidepression meds
nessasary but not sufficient for cure
26
why might adding serotonin with drug not lead to increased serotonin in brain for awhile?
takes a while for auto receptors to habituate (down regulate auto receptors)
27
what do antidepressants do to postsynaptic receptors
With chronic treatment, antidepres-sants are able to enhance the sensitivity and functioning of 5-HT1A postsynaptic receptors, leading to increased mono-amine activity
28
where does the 5-HT system in the brain run
from the raphe nuclei through the medial forebrain bundle to the forebrain
29
... activity is also dysregu-lated in depression
NE
30
what other NT could influence depression (not monoamine theory
GABA, acetylcholine, opioid peptides, and cannabinoids, and the balance achieved among levels of these neurotransmitters
31
T: an important part of the neuroendocrine system that controls the body’s response to stress.
HPA axis
32
what are the 5 stages of a stress response in HPA axis
CRH released in hypothalamus
ACTH from anterior pituitary
secretion of cortisol in adrenal glands
33
HPA axis is always active
f after stress in fight or flight ends it should stop through negative feedback to hypo to stop releasing CRH
34
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
glucocorticoid theory of depression
35
neurons that contain CRH are in what parts of brain
hypo and limbic system (mood)
36
what are the limbic areas 7
amygdala, hippocampus, thalamus, hypothalamus, basal ganglia, and cingulate gyrus
37
A very common finding in patients with depression is structural change in areas of the limbic sys-tem
t
38
The hypothalamic–pituitary–adrenal axis image on p. 295
review
39
what brain areas looses volume in depression
prefrontal and hippocampus
40
what increases volume with depression
Amygdala
41
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, = .......
heightened stress hormone release
42
therapeutic potential of CRH receptor antagonists?
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
43
how are these 2 theories of depression related
stress hormoones interact with monoamine systems
44
how does cortisol influence monoamine systems
more Da release= up regulation of dopamine receptors in VTA
45
T: anti reward system
stress sytem
46
what accounts for the depressive anxious symptoms of withdrawal
sensitization fo the stress system leads to depressive symptoms
47
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
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)
48
Changes in glucocorticoid levels are also strongly associated with changes in 5-HT function
stress and reduction of 5HT in the hippocampus
49
(the surgical removal of the adrenal glands, thereby clearing the body of cortisol does what to 5 HT
increases receptor densities and binding
50
if 5 HT levels are changed by stressful life events is there any genetic component
certain individuals are genetically predisposed to develop HPA-axis hyperactivity (short 5 HT
51
what does early stressful experiences do to HPA response later in life
primes it to overreact
52
Antidepressant medications reduce HPA-axis activity by increasing the number of ... receptors to create more efficient negative-feedback loops
cortisol
53
nor-malizing the stress response may be a necessary condition in order for antidepressants to work
t
54
what are the 2 first ten antidepressants
MAOIs and tricyclic antidepressants
55
the first MAOI was first a ... treatment
TB
56
are MAOIs still effective in treating depression
yes
57
how do the tricyclics get their name
r molecular structure contains three rings of atoms
58
why did MAOIs loose popularity for awhile
liver damage on too high doses
59
what were the second generation antidepressants
SSRIs
60
most well known SSRI
prozac (similar structure to tricyclics but less side effects also treated anxiety)
61
other name for third gen antidepressants
atypical SNRIs
62
the stimulation of the rhiticular formation NE activity helps what depression symptoms
fatigue and loss of energy
63
3 main drug classes of antidepressants
MAOIs
trycyclics
SSRIs
64
what does SNDRIs stand for
Triple monoamine reuptake inhibitors, also known as sero-tonin-norepinephrine-dopamine reuptake inhibitors
65
how do the different antidepressants classes differ in absorption
similar
66
put in order of faster to slowest absorption
TCAs
| SSRIs and SNRIs
67
Antidepressants generally have low levels of protein binding
f high
68
TCAs: first pass metabolism is inhibited by alcohol what does this do to antidepressants
more absorption (doesn't happen for SSR and NIs)
69
SSRis should not be combined with alcohol
f can be used to treat it
70
how easily do antidepressants cross the blood brain barrier
readily
71
where do antidepressants get concentrated in distribution 4
lungs, kidneys, liver, and brain
72
how do the half lives of the antidepressants compare
MAOIs short 2-4 hours
second and third gen
TACs 24 hours
73
how do half lives influence how often you have to take dose of antidepressants
13.4.3 elimination ??
74
do SSRIs have active metabolites
no
75
how do inidivudals differ in the pharmacokinetics of antidepressants
some people don't have emzymes to destroy drugs = extremely long half lives, can build to toxic level
ethnicity influence enzymes
76
why the lag between antidepressants admin and alleviation of symptoms
neuroadaptations that must take place (specifi-cally, the downregulation of 5-HT1A autoreceptors and increase in serotonin system function
77
All monoamine neurons produce the enzyme ...
monoamine oxidase (MAO)
78
what does monoamine oxidase (MAO) do
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
so what do MAOIs do
block monoamine oxidase (MAO)to up monoamine levels (increase the availability and activity of DA, NE, and 5-HT)
80
what are the 2 types of MAO
MAO A
| MAOB
81
What does MAOA do
degrades all three monoamines
82
what does MAO B do
most active in metabolizing DA
83
why did the unselective MAOIs produce unpleasant side effects
Because both forms of MAO enzymes are present throughout the body`
84
what do newer MAOIs selectively act on
MAO-B at low doses but, at higher doses, also affect MAO-A
85
T: they can detach from MAO rather than deac-tivate it permanently.
reversible
86
Trycylics act similarly to MAOis as first gen
f more like SSRIs
87
what is the mechanism of action for tricyclics
block reuptake transporter proteins on the axon terminals of 5-HT and NE neurons
88
do all tricyclics act the same
no various effects
89
do tricyclics have side effects
additional actions mean they have unpleasant sometimes dangerous side effects
90
the SSRIs effect all monomies just 5 HT more
f
91
can SSRIs select which 5 HT receptor to bind to
SSRIs are not selective with regard to the subtype of serotonin receptor to which they bind
92
. 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 ...
5-HT1A receptor
| 5-HT2 receptors.
93
bupropion is which types of antidepressants
atypical
94
RIs and atypicals do what to 5HT, dopamine and nonep
block the reuptake of 5-HT, NE, and in some cases DA
95
what's another way ayticals may work
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
how is the effect of blocking histamine receptors
induce sedation and drowsiness = treats insomnia component of depression
97
side effects of MAOIs
tremors, weight gain, blurry vision, dry mouth, low blood pressure
98
T: MAOI side effect dizziness or fainting when moving to a standing position after being seated or lying down
postural hypertension
99
when are MAOIs dangerous
with other drugs or foods
100
MAOIs can increase the power of MDMA and cocaine (monoamine-stimulating drugs) why these drugs
they rely on the enzymes that MAOIs block
101
MAOIs also potentiate the ... effects of heroin
hypotensive and CNS-depressant
102
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
seretonin syndrome
103
what are the symptoms of serotonin syndrome
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
what causes serotonin syndrome
acute dramatic increases in serotonin transmutation
105
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
washout (more common when switching from antidepressants with long half life)
106
substance found in food that relies on monoamine oxidase
tyramine
107
what foods is tyramine in
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
what happens if you eat tyramine rich foods while on MAOIs
it doesn't break down and accumulates
109
tyramine when not Brocken down crosses the blood brain barrier influencing CNS
f it is capable of stimulating the release of catechol-amines (NE and E) in the peripheral nervous system
110
T: are hormones made by your adrenal glands, which are located on top of your kidneys sent into blood when stressed
catecholamines
111
what are the behavioural effects of tyramine build up
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
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
cheese effect
113
is selectively avoiding the MAO B enough to let you digest tyramine
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
when is the best time to take MAOIs in comparison to eating
long after eating so tyramine can be metabolized
115
The tricyclics also affect autonomic nervous system functioning through their ...
anticholinergic effects
116
agent is a substance that blocks the action of the neurotransmitter acetylcholine at synapses in the central and the peripheral nervous system:T
anticholinergic
117
TCAs inhibit the ... division of the autonomic nervous system, which uses ACh as a trans-mitter.
parasympathetic
118
what are the effects of TCAs parasympathetic inhibition
dry mouth, constipation, blurred vision, ringing in the ears, and urine retention, excessive sweating, weight gain .
119
Parkinsonian symptoms are similar to
| the side effects of ...
antipsychotics
120
why do TCAs cause weight gain
This may be due to the influence of TCAs on hista-mine activity
121
side effect of which antidepressants: reduction in seizure threshold, which can cause convulsions, especially in those with pre-existing seizure disorders
TCA
122
which antidepressants has least side effects and why
The SSRIs have fewer nonspecific actions on systems
| outside of serotonin
123
side effects of SSRIs
intestine problems, headaches, dizziness, sweating, nervousness, and agitation, but these symptoms tend to dissipate with time.
124
what do SSRIs do to appetite
decrease it
125
what causes the side effects from third gen medications
due to this class’s antagonism of acetylcholine and histamine receptors and enhancement of 5-HT2–3
receptor activity
126
what are the side effects of third gen
increased appetite and weight gain, changes in blood pres-sure, dizziness, dry mouth, and gastrointestinal problems.
127
what 3rd gen antidepressants increases the risk for seizure
bupropin
128
which class of antidepressants is most effective
roughly the same for all but individual differences
129
which antidepressants would you use if you also had anxiety
SSRI or SNRI
130
why are there so many antidepressants available
side effects differ for people
131
why : SSRIs are far superior to any other antidepressants in terms of patients’ remaining compliant to chronic drug regimens
low unwanted side effects
132
mere expectation of improvement can account for up to ..% of the improvement that actu-ally occurs
75
133
why is the placebo effect growing
expectancy effects due to increased belief that they work
134
in patients experiencing mild or moderate depression, placebos and antidepressants are equally effective in alleviating symptoms
t
135
in the most extreme cases of depression antidepressants are more effective
is due to a decreased effectiveness of the placebo rather than an increased effectiveness of the anti-depressant
136
for adolescence which antidepressants work
SSRI
137
what are some of the side effects adolescence experience in response to SSRIs
agitation, hyperactivity, and symptoms of mania
138
antidepressants are reinforcing due to pleasant effects experienced
f not self administers
139
the antidepressants that work on dopamine produce euphoria
f low increases achieved slowly
140
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?
debate
141
which antidepressants effect sleep
all
142
what do the MAOIs do the sleep
cause either insomnia or sedation.
143
what do the trycyclics do the sleep
driowsiness (from anticholinergic properties of drug) used treat insomnia but doesn't increase total sleep time
144
effects of fluoxetine and venlaxafine on sleep?
reduce REM= improve depression
145
why do third gen cause sedation and sleepiness
have antihista-minergic actions and cause sedation and sleepiness, while others, like bupropion, can produce insomnia.
146
why do third gen cause sedation and sleepiness
have antihista-minergic actions and cause sedation and sleepiness, while others, like bupropion, can produce insomnia.
147
how do TCAs influence performance
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
how did SNRIs and SSRIs compare in working memory performance
both improved SNRIs more
149
how do MAOIs influence performance
impairs psychomotor performance
150
TACs and SSRIs cause impaired driving
more collisions t
151
can you develop tolerance to antidepressants? to their side effects?
debate
| after several weeks tolerate side effects except for fatigue with SSRIs
152
do TCAs give you withdrawal? what is it like?
at high doses
| restlessness, anxiety, chills, akathisia, and muscle aches
153
do SSRIs give you withdrawal? what is it like?
dizziness, light-headedness, insomnia, fatigue, anxiety, nausea, headache, and sensory disturbances
154
do SNRIs give you withdrawal? what is it like?
can be serious and include both bodily symptoms, such as heart palpitations and nausea, and psychiatric symptoms including delusions.
155
what are the harmful effects of antidepressants
reproduction
156
how do antidepressants influence sexual functioning
difficulty achieving orgasm
157
the difficulty achieving orgasm is caused by sedation and fatigue
f
158
which antidepressants is not associated with sexual dysfunction and why
bupropion does not effect 5 HT may even enhance due to dopamine
159
how do antidepressants influence the fetus
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
fluoxetine, a SSRI is correlated with intense, violent suicidal preoccupations in some patients
t
161
without antidepressants people were twice as likely as those taking placebos to have sui-cidal ideations and to attempt suicide
f those taking antidepressant medications twice as likely (in young adults mostly)
162
fluoxetine may induce an activating effect marked by racing thoughts, nervousness, and tremor what kind of antidepressants
SSRI
163
T: a move-ment disorder characterized by restlessness, agitation, an inability to sit still, and a compulsion to be continuously active.
akathisia (associated with fluoxetine)
164
can you overdose on antidepressants
second and third gen safer = rare to overdose but can be dangerous though serotonin syndrome
165
dangers of TCAs?
toxic due to their their effect on the contractility of the heart muscle
166
what are treatments for depression other than antidepressants
St johns wart
herbal treatments
light therapy, yoga, acupuncture, mindfulness-based therapy, and sleep-deprivation
167
how effective is ECT
result in neurogenesis counteract cell death caused by cortisol
168
high circulating levels of cortisol and may, in turn, facilitate hyperactivity of the ...stress response in a sort of perpetually damaging feedback loop.
HPA-axis
169
ECT increases BDNF levels and neurogene-sis in these regions, as do antidepressant drugs what is BDNF
protein: brain derived neurotopic factor (BDNF)
170
other brain stimulating methods of treating? 2
transcranial magnetic stimulation and Deep brain stim
171
exercise treats depression, how 2
promotion of hippocampal neurogene-sis, increases in 5-HT and BDNF levels, and a decrease in HPA-axis activity and cortisol production
172
normalization of amygdala activity, and improved PFC–limbic connectivity, Serotonin trans-porter protein levels also show normalization after a year of ...
psychodynamic therapy
