Depressive and Bipolar Disorders Flashcards
what is disruptive mood regulationdisorder
→ Severe recurrent verbal or behavioural temper outbursts out of proportion with intensity to the situation
→ Outbursts inconsistent with developmental level
→ Outbursts 3-5 times a week
→ Mood b/w outbursts is irritable/ angry most of the day, nearly everyday
How long do the symptoms of disruptive mood regulation disorder have to be present before diagnosis
criteria met for a year (12 mth) with no period 3+ mths in which all the criteria weren’t met
What is the age of onset for disruptive mood regulation disorder?
Age of onset = before 10 but NOT before 6 or after 18 (b/w 6-18)
can disruptive mood regulation disorder occur exclusively during a major depressive episode?
NO
What disorders can’t DMRD co occur with?
• Cannot co-exist with Oppositional Defiance Disorder, bipolar or intermittent explosive disorder
what do kids with DMRD tend to develop in adulthood
tend to develop unipolar depressive disorder, or anxiety disorders, rather than bipolar disorder (if they develop anything at all)
second to anxiety _________ is the largest area of mental order diagnosis
Major Depressive Disorder
DSM-5 criteria for depression
→ 5 of the following during 2-wk period
• Depressed mood
• Anhedonia
• weight loss (not dieting) or gain
• Insomnia or hypersomnia
• Psychomotor agitation (enhancement) or retardation (slower movement)
• Fatigue/loss of energy
• Feelings or worthlessness or guilt
• Reduced concentration, indecisiveness
• thoughts of death (suicidal idealization)
what is anhedonia
• Diminished interest or pleasure
What two symptoms must be present to diagnose MDD
depressed mood or anhedonia
what distinguishes depression from bipolar
presence of a manic or hypomanic episode
Criteria for Bipolar I is one manic episode lasting at least a week with 3 or more of the following criteria…
o Inflated self-esteem/ grandiosity
o Reduced need for sleep
o talkative/ pressure to keep talking
o Flight of ideas/ racing thoughts
o Distractibility
o Increased goal-directed activity/psychomotor agitation
o involvement in activities with high risk (gambling, excessive sexual behaviour, spending money, giving gifts)
o impairment in social or occupational functioning, or requires hospitalization or has psychotic features
is a depressive episode required to diagnose bipolar disorder?
NO but it is typically the case
What is the difference b/w bipolar I and II
1: with manic episode
2 (milder version of 1):with hypomanic episode
difference b/w manic episode and hypomanic episode
• same as manic accept NO marked impairment in social or occupational functioning, or hospitalization to prevent harm to self or others, or psychotic features.
What is the point prevalence for Major depression?
5-9%(females), 2-4%(males)
What is the lifetime prevalence of Major depression?
10-20% (females), 5-12% (males)
What is the average age of onset for MDD?
20s-50s, mean=late 30s
Biases for MDD?
No race, SES, or class bias
What is the lifetime prevalence for Bipolar disorder
1-2% no sex bias
what is the age of onset for BD
Late teens – 20s
Canadian Annual prevalence of mood disorders
Females: 6.3%, Males: 4.2%, Overall: 5.2%
Psychodynamic Etiology of depression
Anger turned inward at an introjected lost love object
Depressive Etiology: Seligman (cognitive)
Attribution based model:
• People with depression have a bias towards internal and negative attribution of events
what are the 3 types of negative attributions for failure described by seligman
o Internal reasons: “something about me”
o Global reasons: “Something very big and important about me”
o Stable reasons: “Something unchanging about me”
What is Beck’s theory of depression (cognitive)
• Presence of depressogenic schemata (selecting and interpreting events that generate depression)
- characterized by unrealistically negative views and systematic errors in logic
What is the negative triad described by Beck
Negative thoughts
o Of the self
o Of the world
o Of the future
What are the systematic errors in logic described by Beck
o Arbitrary interference
o Selective abstraction
o Magnification & Minimization
o Overgeneralization
What is Arbitrary Interference
tendency to draw negative conclusions in the face of no evidence whatsoever or contrary evidence
What is Selective abstraction
picking and choosing from among the evidence things that cast your circumstances in a negative light
What is Magnification & Minimization
minimizing positive and maximizing the impact of the negatives
What is Overgeneralization
tendency to see one failure in one circumstance as having broad implications for your entire life
Who developed CBT
Beck
What is the amine hypothesis
- Depression = Low levels of amine neurotransmitter activity
* Mania = High levels of amine neurotransmitter activity
What are the 3 candidate neurotransmitters for depression
o Dopamine
o Noradrenaline
o Serotonin
What are tricyclics?
Inhibit reuptake (blocks reuptake of neurotransmitters into presynaptic neuron, they are left in the synapse longer and remain active)
What are MOA inhibitors
Inhibit breakdown (inhibit monoamine oxidase – which breaks down neurotransmitter molecules)
What does ECT do?
Reduce B-adrenergic receptors; increase serotonergic response, theta-adrenergic receptors (relaxation, inhibition)
What does lithium do?
Stabilizes serotonergic activity
What are precursors?
manufacture more neurotransmitter - increased precursors should improve depression
What are Metabolites?
chemical products left over after neurotransmitters have been broken down - expect them to be lower in depressed patients
What evidence was found when giving patients the precursor L-DOPA
o Enhances effect of MAO inhibitors (consistent with hypothesis)
o May lead to hypomania in BD
What evidence was found with Metabolite: HVA (Homovanillic acid)
o HVA is not lower in CSF of depressed patients (as would have been expected)
o We do see a relation of lower HVA and motor retardation
What neurotransmitter is implicated in motoric symptoms
Dopamine (makes sense because they are implicated in Parkinson’s and other motor disorders)
What evidence was found through norepinephrine metabolite MHPG
o Lower levels of urinary MHPG in depression than controls
o Especially in bipolar patients
What evidence was found through the serotonin Precurser Tryptophan?
o May be antidepressant in mild cases
o Moderate-severe doesn’t work
What evidence was found through the serotonin Metabolite 5-HIAA
- lower CSF levels of 5-HIAA in depression
- Low CSF levels of 5-HIAA in aggression, impulsivity, suicide
what is the theory of permissive serotonin? Evidence?
- Serotonin (master regulator) regulates neural activity of dopamine and norepinephrine
- Reduced regulation = wider activity changes → mania or depression
- Serotonin stabilization by lithium in bipolar disorders (stabilizes the swings of dopamine and norepinephrine)
- Reports of successful treatment with serotonin precursors
What are some problems with the evidence we have gathered based on neurotransmission
- the whole spinal cord and other organs also produces metabolites which can be found in the CSF
- other drugs relieve depression without amine uptake effects
- Delay between drug effects (neurotransmitter activity levels = 1-2 days) and lifting of depression (3-4 weeks)
What are the problems with using drugs that change neurotransmitter levels
Equally likely that it’s the changes in affect that cause changes in neurotransmitters
ex. CBT without drugs is more effective
what are some structural and functional differences in the brains of depressed patients?
- smaller hippocampal volume
- less left frontal EEG activity (more asymmetry) associated with reduced positive emotions
bipolar and unipolar depression are associated with high levels of what?
Cortisol (stress hormone)
how do cortisol release patterns differ during depression
o Release stars earlier in depression (normally 4am – noon, 1am for depression)
o Higher peaks in depression
o Longer release period in depression
o Increased ACTH release by pituitary
What is somatostatin and how is it related to depression
Gut neuropeptide that inhibits HPA axis - low CSF levels in depression = HPA axis more active = more cortisol
what is the concordance rate of 1st degree relatives for depression
6 – 40%
______ are Good as antidepressants when no comorbid anxiety
Omega-3 acids
what is ketamine?
tranquilizer used in veterinary practice: At lower doses than anesthesia does provide rapid relief of depression unlike SSRIs and MOA inhibitors
list drugs for depression
SSRIs, MAO inhibitors, Omega-3 acids, ketamine
what are the physical treatments for depression
- Electroshock Therapy - memory loss
- Transcranial Magnetic Stimulation (brain subjected to magnetic feild - similar to ECT, experimental)
- Deep brain stimulation (brain surgery to inject electrodes)
Where are electrodes injected during Deep brain stimulation
inside the nucleus accumbens, beneath frontal lobes. (related to release of dopamine)
what are psychological treatments of depression?
- Psychodynamic psychotherapy
* Cognitive Behavioural therapy
Pharmacological treatment for bipolar
• Chlorpromazine
• Haloperidol – dopamine antagonist
• Lithium – works for most patients, very rapid.
- side effects
Seligman’s learned hopelessness model of depression the individual becomes depressed when he or she
comes to believe that aversive or negative events are caused by something pervasive about themselves.
