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MOOD DISORDERS > Depression 4 > Flashcards

Depression 4 Flashcards

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1
Q

Generally decreased or asymmetrical _______, decreased ______, lesioned _______ integrity in _______ areas.

A

prefrontal activity, volume, white matter, prefrontal cortex

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2
Q

Prefrontal regions –> _____ functions, cognitive control of _______.

Higher levels of these ______ predict _______ clinical outcomes –> decreased ______

A

executive, behavior

“changes”, poorer, volume

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3
Q

Anterior cingulate cortex –> _______ learning, _______, interface of _______/_______/_______

Higher _______ and decreased _______ in depressed patients

A

reward-based, impulsivity, decision-making, attentions, emotion

activation, volume

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4
Q

Ventral tegmental area (VTA) / nucleus accumbens –> ______, _______ processing, _______ center – ______ in activity of depressed patients.

A

motivation, reward, prediction-dopamine, deficits

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5
Q

Hippocampus –> ________ learning, _______, forms connections with brain regions involved in _______ info;

very responsive to ______ -> decreased ______ in depressed patients.

A

Emotional, memory, emotional-related, stress, volume

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6
Q

Hippocampus is correlated with number of ______, lifetime _______, _______ treatment.

A

episodes, duration, antidepressant

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7
Q

Amygdala –> attention to _______ emotional ______, responds to _______ stimuli, encodes _______ memories

______ activation and _______ in anatomical _______ in depressed patients.

A

negative, regulation, threatening, emotional

Increased, increases, changes

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8
Q

Thalamus is a ______” from _______ regions to ______ regions, and regulates ______ and ______.

Decreased _____ in individuals with depression

A

“relay station, subcortical, cortical, sleep, wakefulness,

size

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9
Q

Neuroplasticity is the ability of neurons and networks of neurons to ______ and ______ over ______ in response to ______.

A

change, adapt, time, stimuli

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10
Q

Neuroplasticity Hypothesis of Depression states ______ neural plasticity leads to ______ seen in ______.

A

dysfunctional, impairments, depression

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11
Q

Stress models of depression show a decrease in ______, reduced connectivity in _____ and ________, but is increased connectivity in the ________.

A

dendritic spine density, PFC, hippocampus, amygdala

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12
Q

Rapid-acting antidepressants, like _______ or ______, as well exercise induce _______.

A

ketamine, SSRIs, dendritic restructuring

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13
Q

Biomarkers that regulate _______ can regulate _______ behaviors

A

synaptic plasticity, depressive-like

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14
Q

Alteration in ______ and ______ of neurons impairs ______ that may lead to depressive symptomology

A

structure, function, functional networks

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15
Q

Neurogenesis is the …..

A

birth of new neurons

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16
Q

Adult neurogenesis has been shown to occur in only two locations ….

A

1) Subventricular zone of the lateral ventricles

2) Dentate gyrus of the hippocampus

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17
Q

Stress can hinder adult …..

A

hippocampal neurogenesis

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18
Q

Antidepressant treatment increases ……

A

hippocampal neurogenesis

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19
Q

Increasing adult neurogenesis can reduce …..

A

depressive-like behaviors

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20
Q

______ neurons in the ______ may restore _______ to improve control of ______ outcomes

A

New, hippocampus, deficits, mood

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21
Q

Apoptosis is the …..

A

induction of cell death

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22
Q

Apoptosis Hypothesis of Depression: Neuronal _____ may be responsible for the _______ changes and _______ seen in depression.

A

loss, volumetric, symptomology,

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23
Q

Stress and depression can induce …..

A

hippocampal apoptosis

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24
Q

Some antidepressants can ______ processes that mediate ______.

A

inhibit, apoptosis

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25
Monoamine Theory of Depression states depression is due to ______ and ______ level ______.
norepinephrine, serotonin, depletion
26
norepinephrine and serotonin are important in (6) ....
mood emotional expression arousal behavioral activity stress aversive signaling
27
Studies have found decreased ________ and decreased ________ to receptors and enzymes
circulating monoamine precursors, serotonin binding
28
Most antidepressants acutely increase _____ levels, but this theory _____ explain why antidepressants take _____ weeks to have any ______.
monoamine, doesn't, 2-6, efficacy
29
Most antidepressants acutely increase _______ which could be due to (3) .....
monoamine levels 1) Altered receptor level 2) Decreased neurotransmitter level 3) Increased degradation
30
The Monoamine Theory of Depression has been the _______, but this is _______.
prevailing theory, changing
31
Dopamine is involved in (5 listed) ......
reward/reinforcement motivational stimuli reward prediction error punishment motor control
32
Depressed people show diminished ______/______ and _______ dysfunction.
interest, motivation, psychomotor
33
Studies have found that ______ in ______ function in “depressed” people and rodents.
changes, dopamine
34
GABA is the main .....
inhibitory neurotransmitters
35
Glutamate is the main ....
excitatory neurotransmitters
36
Depressed peoples have decreased density of _______ interneurons, and decreased _______ levels.
GABAergic, glutamate
37
Depressed people have altered .......
frontal cortex excitability
38
GABA and Glutamate heavily influence _______ and most likely disruption in these affects the ______ of networks.
synaptic plasticity, connectivity
39
_______ targets the glutamate system
Ketamine
40
Stepped-Care Model is least ______, most ______ intervention is provided ______, then if not ______, move on to the next one.
intrusive, “effective”, first, effective
41
Order of Stepped-care Model is (5 steps) .......
1) Behavioral Therapy 2) SSRIs, NRIs, SNRIs 3) Tricyclic / tetracyclic antidepressants 4) MAO irreversible inhibitors 5) Then “treatment-resistant” treatments
42
With Stepped-care Model the order is not determined based on ______, but the order is due to number of ________ associated with each _______
efficacy, side effects, medication
43
Generally all typical antidepressant medications have a ______ remission, and show increase _______ of _______. After withdrawal, ______ relapse rate.
15-30%, response rates, 45-75%, 70-90%
44
The Stepped-Care Model is changing due to uncovering _______, potential new _______ medications / _______ treatments, and the _______ of the cases.
specifiers, atypical, brain stimulation, severity
45
Placebo effectevness depends on (3) ....
1) baseline severity 2) nature of the study population 3) short-term vs. long-term outcomes
46
Antidepressants can increase the risk for ______, not for the actual ______, but potentially for _______ and ______.
suicide, act, suicidal ideation, self-injury
47
Antidepressants increase risk of suicide is usually in the _______ of treatment in _______ populations
early stages, younger
48
_______ antidepressant use reduces the risk of suicide
Longer-term
49
Early antidepressants use in _______ people can _______ energy, irritability, agitation, insomnia
young, increase
50
Why choose medication over psychotherapy? (4)
1) effort 2) time 3) money 4) availability of therapists skilled in CTB or other domains
51
Typical antidepressants have a .....
therapeutic lag
52
Typical antidepressants take roughly _______ after taking the medication to see any ______ of symptoms
2-6 weeks, alleviation
53
Therapeutic lag can also depend on getting the ......
dose correct
54
Therapeutic lag is important to keep in mind especially when we need to treat the disorder .....
as quick as possible
55
Therapeutic lag is also important to keep in mind especially if patients are ______ responding to the prescribed ______.
not, medication
56
Common treatment strategy for typical antidepressants is to treat ______ months then ______; Longer the treatment, typically less risk to _______.
6-12, taper off, relapse
57
Typically all antidepressants can produce ______.
discontinuation syndrome,
58
Discontinuation syndrome is more likely to occur with longer _______ of treatment, and shorter ______ of the drug _______ this.
duration, half life, increases
59
Discontinuation syndrome is similar to ....
mild withdrawal effects
60
Typically all antidepressants can cause......
serotonin syndrome
61
when ______ antidepressants or dose, or compounded drugs on top of each other = built up ______ levels in body that can lead to minor _______ or even _______.
switching, serotonin, side effects, death
62
Usually if _____ medications, wait ______ days as drugs impact ______ levels ______ days after taking the drug (SSRIs may be particularly ______ than other medications for this).
switching, 14 days, serotonin, 7-21, worse
63
Typical antidepressants in the short term typically ______ neurotransmitter levels.
increase
64
Typical antidepressants in the long term is still not _______: Potentially increasing _______, enhancing _______, stopping _______, ”rebalancing” _________ components
definitive, neurogenesis, synaptic plasticity, apoptosis, neurotransmitter
65
Tricyclic antidepressants were created in the ......
1950s
66
tricyclic antidepressants may be better ______ for depression with .....
suited, melancholic features
67
With tricyclic antidepressants, you have to .....
experiment with dose
68
tricyclic antidepressants side effects include .....
dry mouth blurred vision hypotension sedation sudden death
69
Monoamine Oxidase Inhibitors were created in the .....
1950s
70
Monoamine Oxidase Inhibitors you have to ......
experiment with dose
71
Monoamine Oxidase Inhibitors are thought to produce more ________, more _______ and have interactions with _______.
side effects, frequently, food/other drugs
72
Monoamine Oxidase Inhibitors are more effective in .....
atypical depression
73
Monoamine Oxidase Inhibitors have the worse _______ out of all the anti-depressant medication
side effects
74
Monoamine Oxidase Inhibitors has shown efficacy in _______ and _______
anxiety, panic disorders
75
Monoamine Oxidase Inhibitors side effects include ......
headaches hypertension insomnia liver disease weight gain hypomania death
76
Re-uptake inhibitors: SSRIs were created in .....
1980/ 90s
77
Re-uptake inhibitors: SSRIs can cause ________ (Potentially _______ out of the antidepressant medications)
Discontinuation syndrome, worse
78
Re-uptake inhibitors: SSRIs -> typically _____ pill a day; safer in the case of _______, more _______.
one, overdosage, well-tolerated
79
Re-uptake inhibitors: SSRIs have efficacy in ______ and _______
anxiety, obsessive compulsive disorders
80
Re-uptake inhibitors: SSRIs have _______ undesirable side effects (a lot less than ______ or ______)
mild, TCAs, MAOis
81
SRI, SNRIS, NRI = blocks ______ = more _______ in the _______
re-uptake transporters, neurotransmitter, synaptic cleft
82
TCAs = blocks _______ = more _______ in the _______: Also block _______, _______, _______ receptors
re-uptake transporters, neurotransmitter, synaptic cleft, serotonin, glutamate, acetycholine
83
MAO inhibitors = irreversibly ______ to and ______ that breaks down ______, _______, and ______ = more neurotransmitter in _______.
bind, inhibit enzymes, serotonin, norepinephrine, dopamine, synaptic cleft
84
reversible _______ could prove beneficial
MAO inhibitors
85
Ketamine was created in ......
2000s
86
Esketamine was created in .....
2019
87
Ketamine/Esketamine has a .......
dissociative anesthetic
88
Ketamine/Esketamine consists of .....
sub-threshold doses
89
With Ketamine/Esketamine, need to see someone to ......
receive treatment
90
Ketamine/Esketamine is _____ (Works in ______; NOT ______) Produce effects within ______ that may last a _______
rapid, hours-day, weeks-months, hours, week or longer
91
Ketamine/Esketamine has fast _______ (half-life is ______, no ________ /________)
metabolic turnover, 3 hours, discontinuation syndrome, withdrawl symptoms
92
Ketamine/Esketamine short-term side effects ....
agitation confusion hallucinogens
93
Ketamine/Esketamine is intended for .......
treatment-resistant depression
94
Ketamine is not ______ vs. Esketamine is ________
FDA-approved, FDA approved
95
Ketamine mechanism is still unknown in terms of .....
long-term effects
96
Ketamine mechanism short-term: blocks ______ at the _____ binding site
NMDA receptor (glutamate), PCP
97
Brain stimulation usually centers around the idea that the ______ modulates deeper ______, and stimulation can ______.
cortex, limbic regions, “reset/ strengthen” it
98
Brain stimulation is used in ...
treatment-resistant depression
99
No single brain region is the ______ in depression, but rather dysfunction may be due to ______ or _______ between _______ brain regions
causal factor, networks, connectivity, different
100
People with depressive disorder show altered _______ among _______
connectivity, multiple networks
101
Default Mode Network is involved in _______. Brain regions that are active when you are ______ engaged in a task. Roles in _______ activity
“wakeful rest”, NOT, self-directed
102
Default Mode Network is more ______ in people with depression when faced ______ pictures
active, negative
103
Affective Network is increased activation at ______ and during an _______ in people with depression
rest, associated task
104
Affective Network–> processing ______ information. Important in _______, ______, ______. Relationship between ______ and ______.
emotional, vigilance, fear, autonomic regulation, mood, emotion
105
Salience Network – detection, integration, and filtering of _______ (may facilitate changing from ______ to _______).
salient stimuli, default mode, cognitive control network
106
Salience Network shows _______ activation in depressed people
decreased
107
Cognitive Control Network - involved in _______ tasks, _______, _______, and ________.
attention-demanding, working memory, reasoning, problem solving
108
Cognitive Control Network showed _______ activation in task-related activity, but _______ when “at rest”.
decreased, increased
109
Electroconvulsive Therapy (ECT) is when a _____ electrical current is passed through a patients _____ via ______ to induce a ______
brief, brain, 2 electrodes, seizure
110
ECT was originally developed in the ______, still ______, ______ is heavily attached to this
1930s, contentious, stigma
111
ECT is usually reserved for patients with _______; potentially earlier for ________ depression
treatment-resistant depression, melancholic, psychotic, or catatonic
112
______ of patients who don’t respond to ______ respond to _____, and seem to respond to _______ better after ECT
50-80%, medications, ECT, medications
113
ECT ______ times per week, ______ treatments
2-3, 6-12
114
ECT treatment accompanied with _______ and _______
muscle relaxants, light anesthetics
115
ECT can actually be highly ______ and less _____ than thought, works ______
effective, toxic, rapidly
116
ECT can be adapted by ______, _______ of treatments, _______ parameters
electrode placement, frequency, electrical
117
ECT side effects include ______ impairment: _______, ________
cognitive, transient postictal disorientation, retrograde/ anterograde amnesia
118
With ECT maintenance is ______ (usually put on _______ after treatment)
required, antidepressants
119
Utilize ECT if _____ response is potentially ______ for _______ patients
rapid, necessary, suicidal
120
Biggest challenge with ECT is changing the public and patient’s _______ surrounding ECT
attitudes / stigma
121
Trans-cranial magnetic stimulation (TMS) is a ______ that uses ______ to cause ______ flow in the brain and _______ neuronal activity
non-invasive neurostimulator, electromagnetic induction, electric current, increase / decrease
122
Trans-cranial magnetic stimulation (TMS) is a _______ form of stimulation (does not cause a _____)
sub-convulsive, seizure
123
Trans-cranial magnetic stimulation (TMS) is FDA-approved for .....
treatment-resistant depression
124
Issues with TMS, it targets ______ of brain
superficial layers

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