Depression 4 Flashcards
Generally decreased or asymmetrical _______, decreased ______, lesioned _______ integrity in _______ areas.
prefrontal activity, volume, white matter, prefrontal cortex
Prefrontal regions –> _____ functions, cognitive control of _______.
Higher levels of these ______ predict _______ clinical outcomes –> decreased ______
executive, behavior
“changes”, poorer, volume
Anterior cingulate cortex –> _______ learning, _______, interface of _______/_______/_______
Higher _______ and decreased _______ in depressed patients
reward-based, impulsivity, decision-making, attentions, emotion
activation, volume
Ventral tegmental area (VTA) / nucleus accumbens –> ______, _______ processing, _______ center – ______ in activity of depressed patients.
motivation, reward, prediction-dopamine, deficits
Hippocampus –> ________ learning, _______, forms connections with brain regions involved in _______ info;
very responsive to ______ -> decreased ______ in depressed patients.
Emotional, memory, emotional-related, stress, volume
Hippocampus is correlated with number of ______, lifetime _______, _______ treatment.
episodes, duration, antidepressant
Amygdala –> attention to _______ emotional ______, responds to _______ stimuli, encodes _______ memories
______ activation and _______ in anatomical _______ in depressed patients.
negative, regulation, threatening, emotional
Increased, increases, changes
Thalamus is a ______” from _______ regions to ______ regions, and regulates ______ and ______.
Decreased _____ in individuals with depression
“relay station, subcortical, cortical, sleep, wakefulness,
size
Neuroplasticity is the ability of neurons and networks of neurons to ______ and ______ over ______ in response to ______.
change, adapt, time, stimuli
Neuroplasticity Hypothesis of Depression states ______ neural plasticity leads to ______ seen in ______.
dysfunctional, impairments, depression
Stress models of depression show a decrease in ______, reduced connectivity in _____ and ________, but is increased connectivity in the ________.
dendritic spine density, PFC, hippocampus, amygdala
Rapid-acting antidepressants, like _______ or ______, as well exercise induce _______.
ketamine, SSRIs, dendritic restructuring
Biomarkers that regulate _______ can regulate _______ behaviors
synaptic plasticity, depressive-like
Alteration in ______ and ______ of neurons impairs ______ that may lead to depressive symptomology
structure, function, functional networks
Neurogenesis is the …..
birth of new neurons
Adult neurogenesis has been shown to occur in only two locations ….
1) Subventricular zone of the lateral ventricles
2) Dentate gyrus of the hippocampus
Stress can hinder adult …..
hippocampal neurogenesis
Antidepressant treatment increases ……
hippocampal neurogenesis
Increasing adult neurogenesis can reduce …..
depressive-like behaviors
______ neurons in the ______ may restore _______ to improve control of ______ outcomes
New, hippocampus, deficits, mood
Apoptosis is the …..
induction of cell death
Apoptosis Hypothesis of Depression: Neuronal _____ may be responsible for the _______ changes and _______ seen in depression.
loss, volumetric, symptomology,
Stress and depression can induce …..
hippocampal apoptosis
Some antidepressants can ______ processes that mediate ______.
inhibit, apoptosis
Monoamine Theory of Depression states depression is due to ______ and ______ level ______.
norepinephrine, serotonin, depletion
norepinephrine and serotonin are important in (6) ….
mood
emotional expression
arousal
behavioral activity
stress
aversive signaling
Studies have found decreased ________ and decreased ________ to receptors and enzymes
circulating monoamine precursors, serotonin binding
Most antidepressants acutely increase _____ levels, but this theory _____ explain why antidepressants take _____ weeks to have any ______.
monoamine, doesn’t, 2-6, efficacy
Most antidepressants acutely increase _______ which could be due to (3) …..
monoamine levels
1) Altered receptor level
2) Decreased neurotransmitter level
3) Increased degradation
The Monoamine Theory of Depression has been the _______, but this is _______.
prevailing theory, changing
Dopamine is involved in (5 listed) ……
reward/reinforcement
motivational stimuli
reward prediction error
punishment
motor control
Depressed people show diminished ______/______ and _______ dysfunction.
interest, motivation, psychomotor
Studies have found that ______ in ______ function in “depressed” people and rodents.
changes, dopamine
GABA is the main …..
inhibitory neurotransmitters
Glutamate is the main ….
excitatory neurotransmitters
Depressed peoples have decreased density of _______ interneurons, and decreased _______ levels.
GABAergic, glutamate
Depressed people have altered …….
frontal cortex excitability
GABA and Glutamate heavily influence _______ and most likely disruption in these affects the ______ of networks.
synaptic plasticity, connectivity
_______ targets the glutamate system
Ketamine
Stepped-Care Model is least ______, most ______ intervention is provided ______, then if not ______, move on to the next one.
intrusive, “effective”, first, effective
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
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
Generally all typical antidepressant medications have a ______ remission, and show increase _______ of _______. After withdrawal, ______ relapse rate.
15-30%, response rates, 45-75%, 70-90%
The Stepped-Care Model is changing due to uncovering _______, potential new _______ medications / _______ treatments, and the _______ of the cases.
specifiers, atypical, brain
stimulation, severity
Placebo effectevness depends on (3) ….
1) baseline severity
2) nature of the study population
3) short-term vs. long-term outcomes
Antidepressants can increase the risk for ______, not for the actual ______, but potentially for _______ and ______.
suicide, act, suicidal ideation, self-injury
Antidepressants increase risk of suicide is usually in the _______ of treatment in _______ populations
early stages, younger
_______ antidepressant use reduces the risk of suicide
Longer-term
Early antidepressants use in _______ people can _______ energy, irritability, agitation, insomnia
young, increase
Why choose medication over psychotherapy? (4)
1) effort
2) time
3) money
4) availability of therapists skilled in CTB or other domains
Typical antidepressants have a …..
therapeutic lag
Typical antidepressants take roughly _______ after taking the medication to see any ______ of symptoms
2-6 weeks, alleviation
Therapeutic lag can also depend on getting the ……
dose correct
Therapeutic lag is important to keep in mind especially when we need to treat the disorder …..
as quick as possible
Therapeutic lag is also important to keep in mind especially if patients are ______ responding to the prescribed ______.
not, medication
Common treatment strategy for typical antidepressants is to treat ______ months then ______;
Longer the treatment, typically less risk to _______.
6-12, taper off, relapse
Typically all antidepressants can produce ______.
discontinuation syndrome,
Discontinuation syndrome is more likely to occur with longer _______ of treatment, and shorter ______ of the drug _______ this.
duration, half life, increases
Discontinuation syndrome is similar to ….
mild withdrawal effects
Typically all antidepressants can cause……
serotonin syndrome
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
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
Typical antidepressants in the short term typically ______ neurotransmitter levels.
increase
Typical antidepressants in the long term is still not _______: Potentially increasing _______, enhancing _______, stopping _______, ”rebalancing”
_________ components
definitive, neurogenesis, synaptic plasticity, apoptosis, neurotransmitter
Tricyclic antidepressants were created in the ……
1950s
tricyclic antidepressants may be better ______ for depression with …..
suited, melancholic features
With tricyclic antidepressants, you have to …..
experiment with dose
tricyclic antidepressants side effects include …..
dry mouth
blurred vision
hypotension
sedation
sudden death
Monoamine Oxidase Inhibitors were created in the …..
1950s
Monoamine Oxidase Inhibitors you have to ……
experiment with dose
Monoamine Oxidase Inhibitors are thought to produce more ________, more _______ and have interactions
with _______.
side effects, frequently, food/other drugs
Monoamine Oxidase Inhibitors are more effective in …..
atypical depression
Monoamine Oxidase Inhibitors have the worse _______ out of all the anti-depressant medication
side effects
Monoamine Oxidase Inhibitors has shown efficacy in _______ and _______
anxiety, panic disorders
Monoamine Oxidase Inhibitors side effects include ……
headaches
hypertension
insomnia
liver disease
weight gain
hypomania
death
Re-uptake inhibitors: SSRIs were created in …..
1980/ 90s
Re-uptake inhibitors: SSRIs can cause ________ (Potentially _______ out of the antidepressant medications)
Discontinuation syndrome, worse
Re-uptake inhibitors: SSRIs -> typically _____ pill a day; safer in the case of _______, more _______.
one, overdosage, well-tolerated
Re-uptake inhibitors: SSRIs have efficacy in ______ and _______
anxiety, obsessive compulsive disorders
Re-uptake inhibitors: SSRIs have _______ undesirable side effects (a lot less than ______ or ______)
mild, TCAs, MAOis
SRI, SNRIS, NRI = blocks ______ = more _______ in the _______
re-uptake transporters, neurotransmitter, synaptic cleft
TCAs = blocks _______ = more
_______ in the _______: Also block _______, _______, _______ receptors
re-uptake transporters, neurotransmitter, synaptic cleft, serotonin, glutamate, acetycholine
MAO inhibitors = irreversibly ______ to and ______ that breaks down ______, _______, and ______ = more neurotransmitter in _______.
bind, inhibit enzymes, serotonin, norepinephrine, dopamine, synaptic cleft
reversible _______ could prove beneficial
MAO inhibitors
Ketamine was created in ……
2000s
Esketamine was created in …..
2019
Ketamine/Esketamine has a …….
dissociative anesthetic
Ketamine/Esketamine consists of …..
sub-threshold doses
With Ketamine/Esketamine, need to see someone to ……
receive treatment
Ketamine/Esketamine is _____ (Works in ______; NOT ______) Produce effects within ______ that may last a _______
rapid, hours-day, weeks-months, hours, week or longer
Ketamine/Esketamine has fast _______ (half-life is ______, no ________ /________)
metabolic turnover, 3 hours, discontinuation syndrome, withdrawl symptoms
Ketamine/Esketamine short-term side effects ….
agitation
confusion
hallucinogens
Ketamine/Esketamine is intended for …….
treatment-resistant depression
Ketamine is not ______ vs. Esketamine is ________
FDA-approved, FDA approved
Ketamine mechanism is still unknown in terms of …..
long-term effects
Ketamine mechanism short-term: blocks ______ at the _____ binding site
NMDA receptor (glutamate), PCP
Brain stimulation usually centers around the idea that the ______ modulates deeper ______, and stimulation can ______.
cortex, limbic regions, “reset/ strengthen” it
Brain stimulation is used in …
treatment-resistant depression
No single brain region is the ______ in depression, but rather dysfunction may be due to ______ or _______ between _______ brain regions
causal factor, networks, connectivity, different
People with depressive disorder show altered _______ among _______
connectivity, multiple networks
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
Default Mode Network is more ______ in people with depression when faced ______ pictures
active, negative
Affective Network is increased activation at ______ and during an _______ in people with depression
rest, associated task
Affective Network–> processing ______ information. Important in _______, ______, ______. Relationship between ______ and ______.
emotional, vigilance, fear, autonomic regulation, mood, emotion
Salience Network – detection, integration, and filtering of _______ (may facilitate changing from ______ to _______).
salient stimuli, default mode, cognitive control network
Salience Network shows _______ activation in depressed people
decreased
Cognitive Control Network - involved in _______ tasks, _______, _______, and ________.
attention-demanding, working
memory, reasoning, problem solving
Cognitive Control Network showed _______ activation in task-related
activity, but _______ when “at rest”.
decreased, increased
Electroconvulsive Therapy (ECT) is when a _____ electrical current is passed through a patients _____ via ______ to induce a ______
brief, brain, 2 electrodes, seizure
ECT was originally developed in the ______, still ______, ______ is heavily attached to this
1930s, contentious, stigma
ECT is usually reserved for patients with _______; potentially earlier for ________ depression
treatment-resistant depression, melancholic, psychotic, or catatonic
______ of patients who don’t respond to ______ respond to _____, and
seem to respond to _______ better after ECT
50-80%, medications, ECT, medications
ECT ______ times per week, ______ treatments
2-3, 6-12
ECT treatment accompanied with _______ and _______
muscle relaxants, light anesthetics
ECT can actually be highly ______ and less _____ than thought, works ______
effective, toxic, rapidly
ECT can be adapted by ______, _______ of treatments, _______ parameters
electrode placement, frequency, electrical
ECT side effects include ______ impairment: _______, ________
cognitive, transient postictal disorientation, retrograde/
anterograde amnesia
With ECT maintenance is ______ (usually put on _______ after treatment)
required, antidepressants
Utilize ECT if _____ response is potentially ______ for _______ patients
rapid, necessary, suicidal
Biggest challenge with ECT is changing the public and patient’s
_______ surrounding ECT
attitudes / stigma
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
Trans-cranial magnetic stimulation (TMS) is a _______ form of stimulation (does not cause a _____)
sub-convulsive, seizure
Trans-cranial magnetic stimulation (TMS) is FDA-approved for …..
treatment-resistant depression
Issues with TMS, it targets ______ of brain
superficial layers