exam 2 lecture notes Flashcards
what needs to be present for a MDE
at least one A symptom and multiple B symptoms that are present for most of the day/more often than not for a 2 week period and overall adds up to at least five symptoms
what is the difference between A1 and A2 symptoms when diagnosing a MDE
A1: gain of negative affect
A2: loss of positive affect
what needs to be present for a MDD
meet criteria for at least one MDE but no mania or hypomania
what are the two types of MDD
single episode
recurrent
when is the onset risk of an MDD
increases dramatically in early teen years
what needs to be present for a PDD
depressed mood for most of the day, more days than not, for 2 years (if under 18 then for 1 year)
- couples with 2 or more B symptoms
when is the usual onset for PDD
early 20s
early onset: before 21
what is the difference between MDD and PDD
MDD: usually shorter depressive episodes
PDD: longer depressive episodes
who created the cognitive model of depression
Beck
what are the four parts of the cognitive model of depression
- vulnerabilities to depressed thinking stems from early learning and cognitive abilities
- vulnerabilities + stress = negative thoughts
- negative thoughts are consolidated into negative beliefs about self, world, future, etc
- core beliefs feed back to bias cognitive processing and responses
what are the three levels of thinking involved in the cognitive model of depression
- depressive core beliefs
- negative core beliefs shape maladaptive cognitive style
- negative core beliefs lead to automatic negative thoughts
what is the usual attribution style with depression
internal
stable
global
what model of depression is supported by functional assessment
behavioral model
what are the steps of depression in the behavioral model
- conditions that contribute to the behavior –> behavior
- what happens after the behavior –> consequences
what is the goal of a functional assessment
to identify triggers for behaviors that lead to depression and replace them with other behaviors
what is behavioral activation
engaging in activities that promote wellness
what model of depression is learned helplessness a part of
behavioral model
what brain systems are involved in depression
ventral striatum
amygdala
ventromedial prefrontal cortex
what needs to be present to meet criteria for a manic episode
combination of criteria A plus 3 or 4 symptoms from criteria B lasting a week or more
what is the criteria that needs to be met for bipolar I disorder
presence of at least one manic episode
what is the age of onset risk period for bipolar disorder I
same as MDD (early teens - risk increases dramatically)
what is the criteria for a hypomanic episode
combination of criteria A plus 3 or 4 symptoms for 4-7 days
(with no hospitalization or significant impairment)
what is the criteria for bipolar II disorder
presence of one or more MDE and at least one hypomanic episode
(no manic episode)
- symptoms can cause a change in functioning but not marked impairment
what will bipolar II disorder usually evolve into
full manic or mixed episode
what are risk factors for mania
major life events
types of stressors will determine if it causes mania or depressive episode
what are reward activating events and what are they likely to trigger
“good stress”
more likely to trigger manic episode
what are failure and rejection type life events more likely to cause
depressive episodes
is it possible to have bipolar disorder without depression
yes but it is very rare
what does serotonin regulate
feeding
mood regulation
stress response
what is serotonin synthesized from
tryptophan
what is serotonin broken down by after it reuptake occurs
MAO
monoamine oxidase
what does MAO break down other than serotonin
NE and dopamine
what are MAOIs
monoamine oxidase inhibitors
(used to treat depression)
what are dual mode antidepressants
specific serotonin/NE reuptake inhibitors (SNRIs)
what kind of depression are medications that target dopamine useful for
anhedonic depression (loss of pleasure or interest)
what is the monoamine hypothesis
increasing synaptic serotonin, NE, dopamine increases mood
what are the benefits of psychotherapy
no side effects
can help with other things other than the main concern
what is behavioral activation therapy
identifying maladaptive behaviors and activities to change them to better behaviors and activities
what is cognitive behavioral therapy/cognitive restructuring
identifying maladaptive thoughts and identifying the automatic relationships with maladaptive thoughts to challenge them and create more adaptive thoughts
what NT are dysregulated with mania symptoms
dopamine
serotonin
NE
GABA
glutamate
how are drug treatments utilized for mania
meds are regulated based on current mood to stabilize the mood
what does lithium cause
decreased NE and glutamate
increased GABA
what does lithium treat and what is a con to using lithium
treats mania but depression
has a small therapeutic window
what two main structures is dopamine released into
basal ganglia
frontal lobe
where is dopamine released in the basal ganglia
mesolimbic pathway: links VTA to ventral striatum
(reinforcement and reward)
where is dopamine released in the frontal lobe
mesocortical system: links VTA to the PFC
(short term memory, planning, problem solving)
what happens to dopamine sensitivity with bipolar disorders
increased sensitivity to dopamine over time
what happens to dopamine sensitivity with unipolar depression
decreased availability of and sensitivity to dopamine
what are three psychological treatments to treat mania
IPSRT (regulating schedule)
cognitive treatments
family focused treatments
what do anxiety disorders include
disorders that share features of excessive fear and anxiety and related behavioral disorders
what kind of stress leads to optimal performance
moderate stress
how do the amygdala and hippocampus stimulate the hypothalamus
amygdala increases hypothalamus stimulation
hippocampus decreases hypothalamus stimulation
what is the biggest difference between fear and anxiety
fear: in the moment fear with a distinct fight/flight response
anxiety: fear about the future with somatic symptoms
how can cognitive vulnerabilities influence anxiety
biases toward stimuli and interpretations where related exposure to stress may trigger fear which is filtered through cognitive biases and ultimately leads to anxiety
what are benzodiazepines
drugs that are GABA agonists and inhibit neurons in the hypothalamus and lead to less signaling from the hypothalamus
what are NE antagonists
drugs that block the receptors where NE likes to bind so there is less stimulation of peripheral systems
what are the 7 different anxiety disorders
panic disorder
agoraphobia
specific phobia
generalized anxiety disorder
social anxiety
OCD
PTSD
what are panic attacks
abrupt surge of intense fear and discomfort that reaches a peak within minutes and coincides with 4+ of the symptoms on the list
what are the 4 criteria for panic disorder
A. recurrent unexpected panic attacks
B. 1 attack or more was followed by 1 month of concern/worry over the panic attack and/or maladaptive change in behavior as a result of the panic attack
C. it is not better explained by another medical condition
D. it is not better explained by another mental disorder
does everyone that experiences panic attacks develop an anxiety disorder
no, only a small percentage
what is the onset of panic disorder
acute onset ages 21-23
what is agoraphobia
A. marked fear/anxiety about 2+ of the situations on the list
B. situations are feared because of thoughts that the situation is unescapable
can panic attacks be conditioned to cause fear and future panic attacks
yes both by classical and operant conditioning
what are cognitive contributions agoraphobia and panic attacks/disorder
catastrophic thoughts: tendency to view bodily sensations as dangerous
what are other contributions agoraphobia and panic attacks/disorder
biological sensitivity to have an “emergency” stress response
social stress
culture
early childhood-insecure attachment
what are the 7 conditions that need to be met for a specific phobia
A. fear/anxiety
B. object/situation always provokes fear/anxiety
C. object/situation is actively avoided
D. fear/anxiety is out of proportion to the actual danger
E. persistent for 6+ months
F. causes distress/impairment
G. not better explained by another mental disorder
what are the characteristics of blood-injection-injury phobia
decreased heart rate and blood pressure
inherited vasovagal response
onset = 9 yrs
what are the characteristics of situational phobia
fear of specific situations
onset early to mid 20s
what is the onset of animal phobias
7 yrs
what is the onset of natural environment phobias
7 yrs
are females or males more likely to have specific phobias
females
what are two treatment options for specific phobias
exposure therapy (classical conditioning)
cognitive restructuring
what are the three main symptoms of GAD
A. excessive anxiety or worry about lots of events more days than now
B. difficulty controlling worry
C. three or more C symptoms
what is the duration for GAD
every day or an hour or more for 6+ months
what is the age of onset of GAD
about 30 but can be gradual
what is the main treatment for GAD
cognitive behavioral therapy
what are the main symptoms of social phobia/SAD
fear/anxiety about 1 or more social situations
feel humiliated, embarrassed, rejected
almost always evokes fear/anxiety
social situations are avoided/endured with fear
anxiety is out of proportion to actual threat
persistent for 6+ months
what is the ratio of M:F for SAD
1:1
what is the age of onset for SAD
~13yrs
what are the two main symptoms of OCD
report obsessions, compulsions, or both
obsessions/compulsions are time consuming (more than 1 hr per day) or cause distress/impairment
what is the M:F ratio of OCD
1:1
what is the age of onset for OCD
males 12-14
females early 20s
what are the specifiers for PTSD
delayed expression
dissociative symptoms
what increases resilience for PTSD
social support
what brain structure is reduced in PTSD
reduced hippocampal volume
what is the stress response in PTSD
cortisol –> hippocampus –> hypothalamus activity
what are the three eating disorders
anorexia nervosa
bulimia nervosa
binge eating disorder
what are the two specifiers for anorexia nervosa
restricting: no binging/purging in past 3 months
binge/purge type: recurrent episodes of binge eating
what is the change that happens in the brain with anorexia nervosa
decreased grey matter
what are two subtypes of binge eating disorder
dieting
negative affect
what is the ventral striatum (nucleus accumbens) involved in
associated with reward
what is the dorsal striatum associated with
learning of habits and skills
what is the basal ganglia composed of
ventral striatum
dorsal striatum
what are pharmacokinetics
process by which drugs are absorbed/distributed in the body
what are the 5 things that affect pharmacokinetics
R routes of administration
A absorption
D distribution in the body
M metabolism/inactivation
E excretion
what three brain regions is dopamine primarily released into
basal ganglia
limbic regions
frontal lobe
what do amphetamines and methamphetamines do to dopamine
cause dopamine terminals to release more dopamine into nucleus accumbens and block reuptake of dopamine
what do nicotine/THC/morphine do to dopamine
stimulate dopamine neurons to fire more action potentials and therefore release more dopamine
what are 5 examples of stimulants
cocaine
amphetamine
methamphetamine
nicotine
caffeine
what does cocaine do to dopamine
increases synaptic levels of dopamine by inhibiting reuptake
what does cocaine do to serotonin and NE
affects reuptake
what three ways do amphetamines effect dopamine
increase dopamine release
block dopamine reuptake
makes dopamine reuptake transporter work backwards
what are the differences between amphetamine and methamphetamine (2)
extra methyl group makes it easier to cross BBB and harder to breakdown
longer half life
what is nicotine an agonist of
nACh receptor
what do ACh receptors do in the CNS
modulate levels of other NTs
ACh release enhances memory and concentration
what do ACh receptors do in the PNS
activate sympathetic nervous system to release epi and NE
what receptors does caffeine block
adenosine receptors
what does caffeine do to serotonin and dopamine
increase both
what are two examples of depressants
barbiturates
alcohol
what do barbiturates do in the brain
reduce GABA signals
what does alcohol do in the brain
GABA-A agonist (inhibitory)
- decreases GABA receptor sensitivity
NMDA antagonist (excitatory)
- NMDA receptors increase level of response and binding sites
what NT do cannabinoids effect
dopamine
what is a prodrome
period of early, lower level symptoms
what is thorazine
dopamine antagonist previously used for treating schizophrenia
what does ketamine or PCP do
block glutamate transmission at NMDA receptors so there will be increased Glu release and increased Glu at AMPA receptors
what kind of symptoms can NMDA receptor antagonists cause
positive and negative symptoms
what are atypical antipsychotics
partly dopamine receptors but lower affinity
high affinity for serotonin and NE receptors
what effects do atypical antipsychotics have
reduce negative symptoms
few motor side effects
more metabolic side effects
