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MOOD DISORDERS > Depression 4 > Flashcards

Depression 4 Flashcards

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
Q

Monoamine Theory of Depression states depression is due to ______ and ______ level ______.

A

norepinephrine, serotonin, depletion

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26
Q

norepinephrine and serotonin are important in (6) ….

A

mood
emotional expression
arousal
behavioral activity
stress
aversive signaling

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27
Q

Studies have found decreased ________ and decreased ________ to receptors and enzymes

A

circulating monoamine precursors, serotonin binding

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28
Q

Most antidepressants acutely increase _____ levels, but this theory _____ explain why antidepressants take _____ weeks to have any ______.

A

monoamine, doesn’t, 2-6, efficacy

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29
Q

Most antidepressants acutely increase _______ which could be due to (3) …..

A

monoamine levels

1) Altered receptor level

2) Decreased neurotransmitter level

3) Increased degradation

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30
Q

The Monoamine Theory of Depression has been the _______, but this is _______.

A

prevailing theory, changing

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31
Q

Dopamine is involved in (5 listed) ……

A

reward/reinforcement

motivational stimuli

reward prediction error

punishment

motor control

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32
Q

Depressed people show diminished ______/______ and _______ dysfunction.

A

interest, motivation, psychomotor

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33
Q

Studies have found that ______ in ______ function in “depressed” people and rodents.

A

changes, dopamine

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34
Q

GABA is the main …..

A

inhibitory neurotransmitters

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35
Q

Glutamate is the main ….

A

excitatory neurotransmitters

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36
Q

Depressed peoples have decreased density of _______ interneurons, and decreased _______ levels.

A

GABAergic, glutamate

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37
Q

Depressed people have altered …….

A

frontal cortex excitability

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38
Q

GABA and Glutamate heavily influence _______ and most likely disruption in these affects the ______ of networks.

A

synaptic plasticity, connectivity

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39
Q

_______ targets the glutamate system

A

Ketamine

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40
Q

Stepped-Care Model is least ______, most ______ intervention is provided ______, then if not ______, move on to the next one.

A

intrusive, “effective”, first, effective

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41
Q

Order of Stepped-care Model is (5 steps) …….

A

1) Behavioral Therapy

2) SSRIs, NRIs, SNRIs

3) Tricyclic / tetracyclic antidepressants

4) MAO irreversible inhibitors

5) Then “treatment-resistant” treatments

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42
Q

With Stepped-care Model the order is not determined based on ______, but the order is due to number of
________ associated with each _______

A

efficacy, side effects, medication

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43
Q

Generally all typical antidepressant medications have a ______ remission, and show increase _______ of _______. After withdrawal, ______ relapse rate.

A

15-30%, response rates, 45-75%, 70-90%

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44
Q

The Stepped-Care Model is changing due to uncovering _______, potential new _______ medications / _______ treatments, and the _______ of the cases.

A

specifiers, atypical, brain
stimulation, severity

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45
Q

Placebo effectevness depends on (3) ….

A

1) baseline severity

2) nature of the study population

3) short-term vs. long-term outcomes

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46
Q

Antidepressants can increase the risk for ______, not for the actual ______, but potentially for _______ and ______.

A

suicide, act, suicidal ideation, self-injury

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47
Q

Antidepressants increase risk of suicide is usually in the _______ of treatment in _______ populations

A

early stages, younger

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48
Q

_______ antidepressant use reduces the risk of suicide

A

Longer-term

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49
Q

Early antidepressants use in _______ people can _______ energy, irritability, agitation, insomnia

A

young, increase

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50
Q

Why choose medication over psychotherapy? (4)

A

1) effort
2) time
3) money
4) availability of therapists skilled in CTB or other domains

51
Q

Typical antidepressants have a …..

A

therapeutic lag

52
Q

Typical antidepressants take roughly _______ after taking the medication to see any ______ of symptoms

A

2-6 weeks, alleviation

53
Q

Therapeutic lag can also depend on getting the ……

A

dose correct

54
Q

Therapeutic lag is important to keep in mind especially when we need to treat the disorder …..

A

as quick as possible

55
Q

Therapeutic lag is also important to keep in mind especially if patients are ______ responding to the prescribed ______.

A

not, medication

56
Q

Common treatment strategy for typical antidepressants is to treat ______ months then ______;

Longer the treatment, typically less risk to _______.

A

6-12, taper off, relapse

57
Q

Typically all antidepressants can produce ______.

A

discontinuation syndrome,

58
Q

Discontinuation syndrome is more likely to occur with longer _______ of treatment, and shorter ______ of the drug _______ this.

A

duration, half life, increases

59
Q

Discontinuation syndrome is similar to ….

A

mild withdrawal effects

60
Q

Typically all antidepressants can cause……

A

serotonin syndrome

61
Q

when ______ antidepressants
or dose, or compounded drugs on top of each other = built up ______ levels in
body that can lead to minor _______ or even _______.

A

switching, serotonin, side effects, death

62
Q

Usually if _____ medications, wait ______ days as drugs impact ______ levels ______ days after taking the drug (SSRIs may be particularly ______ than other medications for this).

A

switching, 14 days, serotonin, 7-21, worse

63
Q

Typical antidepressants in the short term typically ______ neurotransmitter levels.

A

increase

64
Q

Typical antidepressants in the long term is still not _______: Potentially increasing _______, enhancing _______, stopping _______, ”rebalancing”
_________ components

A

definitive, neurogenesis, synaptic plasticity, apoptosis, neurotransmitter

65
Q

Tricyclic antidepressants were created in the ……

A

1950s

66
Q

tricyclic antidepressants may be better ______ for depression with …..

A

suited, melancholic features

67
Q

With tricyclic antidepressants, you have to …..

A

experiment with dose

68
Q

tricyclic antidepressants side effects include …..

A

dry mouth
blurred vision
hypotension
sedation
sudden death

69
Q

Monoamine Oxidase Inhibitors were created in the …..

A

1950s

70
Q

Monoamine Oxidase Inhibitors you have to ……

A

experiment with dose

71
Q

Monoamine Oxidase Inhibitors are thought to produce more ________, more _______ and have interactions
with _______.

A

side effects, frequently, food/other drugs

72
Q

Monoamine Oxidase Inhibitors are more effective in …..

A

atypical depression

73
Q

Monoamine Oxidase Inhibitors have the worse _______ out of all the anti-depressant medication

A

side effects

74
Q

Monoamine Oxidase Inhibitors has shown efficacy in _______ and _______

A

anxiety, panic disorders

75
Q

Monoamine Oxidase Inhibitors side effects include ……

A

headaches
hypertension
insomnia
liver disease
weight gain
hypomania
death

76
Q

Re-uptake inhibitors: SSRIs were created in …..

A

1980/ 90s

77
Q

Re-uptake inhibitors: SSRIs can cause ________ (Potentially _______ out of the antidepressant medications)

A

Discontinuation syndrome, worse

78
Q

Re-uptake inhibitors: SSRIs -> typically _____ pill a day; safer in the case of _______, more _______.

A

one, overdosage, well-tolerated

79
Q

Re-uptake inhibitors: SSRIs have efficacy in ______ and _______

A

anxiety, obsessive compulsive disorders

80
Q

Re-uptake inhibitors: SSRIs have _______ undesirable side effects (a lot less than ______ or ______)

A

mild, TCAs, MAOis

81
Q

SRI, SNRIS, NRI = blocks ______ = more _______ in the _______

A

re-uptake transporters, neurotransmitter, synaptic cleft

82
Q

TCAs = blocks _______ = more
_______ in the _______: Also block _______, _______, _______ receptors

A

re-uptake transporters, neurotransmitter, synaptic cleft, serotonin, glutamate, acetycholine

83
Q

MAO inhibitors = irreversibly ______ to and ______ that breaks down ______, _______, and ______ = more neurotransmitter in _______.

A

bind, inhibit enzymes, serotonin, norepinephrine, dopamine, synaptic cleft

84
Q

reversible _______ could prove beneficial

A

MAO inhibitors

85
Q

Ketamine was created in ……

A

2000s

86
Q

Esketamine was created in …..

A

2019

87
Q

Ketamine/Esketamine has a …….

A

dissociative anesthetic

88
Q

Ketamine/Esketamine consists of …..

A

sub-threshold doses

89
Q

With Ketamine/Esketamine, need to see someone to ……

A

receive treatment

90
Q

Ketamine/Esketamine is _____ (Works in ______; NOT ______) Produce effects within ______ that may last a _______

A

rapid, hours-day, weeks-months, hours, week or longer

91
Q

Ketamine/Esketamine has fast _______ (half-life is ______, no ________ /________)

A

metabolic turnover, 3 hours, discontinuation syndrome, withdrawl symptoms

92
Q

Ketamine/Esketamine short-term side effects ….

A

agitation
confusion
hallucinogens

93
Q

Ketamine/Esketamine is intended for …….

A

treatment-resistant depression

94
Q

Ketamine is not ______ vs. Esketamine is ________

A

FDA-approved, FDA approved

95
Q

Ketamine mechanism is still unknown in terms of …..

A

long-term effects

96
Q

Ketamine mechanism short-term: blocks ______ at the _____ binding site

A

NMDA receptor (glutamate), PCP

97
Q

Brain stimulation usually centers around the idea that the ______ modulates deeper ______, and stimulation can ______.

A

cortex, limbic regions, “reset/ strengthen” it

98
Q

Brain stimulation is used in …

A

treatment-resistant depression

99
Q

No single brain region is the ______ in depression, but rather dysfunction may be due to ______ or _______ between _______ brain regions

A

causal factor, networks, connectivity, different

100
Q

People with depressive disorder show altered _______ among _______

A

connectivity, multiple networks

101
Q

Default Mode Network is involved in _______. Brain regions that are
active when you are ______ engaged in a task. Roles in _______ activity

A

“wakeful rest”, NOT, self-directed

102
Q

Default Mode Network is more ______ in people with depression when faced ______ pictures

A

active, negative

103
Q

Affective Network is increased activation at ______ and during an _______ in people with depression

A

rest, associated task

104
Q

Affective Network–> processing ______ information. Important in _______, ______, ______. Relationship between ______ and ______.

A

emotional, vigilance, fear, autonomic regulation, mood, emotion

105
Q

Salience Network – detection, integration, and filtering of _______ (may facilitate changing from ______ to _______).

A

salient stimuli, default mode, cognitive control network

106
Q

Salience Network shows _______ activation in depressed people

A

decreased

107
Q

Cognitive Control Network - involved in _______ tasks, _______, _______, and ________.

A

attention-demanding, working
memory, reasoning, problem solving

108
Q

Cognitive Control Network showed _______ activation in task-related
activity, but _______ when “at rest”.

A

decreased, increased

109
Q

Electroconvulsive Therapy (ECT) is when a _____ electrical current is passed through a patients _____ via ______ to induce a ______

A

brief, brain, 2 electrodes, seizure

110
Q

ECT was originally developed in the ______, still ______, ______ is heavily attached to this

A

1930s, contentious, stigma

111
Q

ECT is usually reserved for patients with _______; potentially earlier for ________ depression

A

treatment-resistant depression, melancholic, psychotic, or catatonic

112
Q

______ of patients who don’t respond to ______ respond to _____, and
seem to respond to _______ better after ECT

A

50-80%, medications, ECT, medications

113
Q

ECT ______ times per week, ______ treatments

A

2-3, 6-12

114
Q

ECT treatment accompanied with _______ and _______

A

muscle relaxants, light anesthetics

115
Q

ECT can actually be highly ______ and less _____ than thought, works ______

A

effective, toxic, rapidly

116
Q

ECT can be adapted by ______, _______ of treatments, _______ parameters

A

electrode placement, frequency, electrical

117
Q

ECT side effects include ______ impairment: _______, ________

A

cognitive, transient postictal disorientation, retrograde/
anterograde amnesia

118
Q

With ECT maintenance is ______ (usually put on _______ after treatment)

A

required, antidepressants

119
Q

Utilize ECT if _____ response is potentially ______ for _______ patients

A

rapid, necessary, suicidal

120
Q

Biggest challenge with ECT is changing the public and patient’s
_______ surrounding ECT

A

attitudes / stigma

121
Q

Trans-cranial magnetic stimulation (TMS) is a ______ that uses ______ to cause ______ flow in the brain and _______ neuronal activity

A

non-invasive neurostimulator, electromagnetic induction, electric current, increase / decrease

122
Q

Trans-cranial magnetic stimulation (TMS) is a _______ form of stimulation (does not cause a _____)

A

sub-convulsive, seizure

123
Q

Trans-cranial magnetic stimulation (TMS) is FDA-approved for …..

A

treatment-resistant depression

124
Q

Issues with TMS, it targets ______ of brain

A

superficial layers

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