Depressive Disorders Flashcards
What are the DSM-5 Depressive Disorders?
Disruptive Mood Dysregulation Disorder
Major Depressive Disorder
Persistant Depressive Disorder (Dysthymia)- 2 years in adults and 1 in children- milder but longer persisting
Premenstural Dysphoric Disorder
Is Disruptive Mood Dysregulation Disorder a new disorder? If so, why was it added?
Yes, so that children wouldn’t be overdiagnosed with bipolar- usually develop unipolar depression or anxiety when older
Can be used to describe problems with anger but problem because only diagnosable before 18 and age of onset should be 10.
What were the DSM- IV ‘Mood Disorders’?
Two groups:
Depressive: Major Depression and Dysthymic Disorder
Bi-polar: I, II and Cyclothymic Disorder
Which depressive disorders in the DSM-5 are new?
Disruptive Mood Dysregulation Disorder and Premenstrual Dysphoric Disorder (used to be in Appendix but now much research on the impact of functioning and treatment-responsiveness)
Major Depressive Disorder Criteria
5 or more (including 1 & 2) of the following in 2 weeks:
- Depressed mood most of the day, nearly every day
- Diminished interest or pleasure
- Weight loss or weight gain
- Insomnia or hypersomnia
- Psychomotor agitation
- Fatigue or loss of energy
- Feelings of worthlessness or guilt
- Diminished ability to concentrate
- Recurrent thoughts of death- suicidal ideation
Persistant Depressive Disorder Criteria
A: Depressed mood more days than not
B:
2 or more of the following: (3-9 of MDD without psychomotor agitation)
1. Loss of appetite or overeating
2. Insomnia or hypersomnia
3. Fatigue or loss of energy
4. Low self-esteem (like worthlessness or guilt)
5. Poor concentration or difficulty making decisions
6. Feelings of hoplessness (milder than suicide)
Specifiers for Depressive Disorders
Anxious Distress- 5 symptoms- severity on how many symp
Melancholic features-lack of pleasure and reactivity
-depressed mood- empty
-worse in the morning
-early-morning awakening (at least 2 hours before usual)
-marked psychomotor agitation or retardation
-significant anorexia or weight loss
-excessive or inappropriate guilt
Atypical features- weight gain, oversleep, rejection sensitivity and mood reactivity
Psychotic features: delusions/hallucinations present
Catatonia
Peripartum onset
Seasonal pattern
Parker’s (2000) alternative subtypes
melancholic, psychotic and non-melancholic (respond to talking therapies and placebos)
mel and psyc- biological, drug treatment, don’t respond to placebo
BUT may just be difference in severity
Prevalence
Lifetime: 16.4%
One-year in Aus: 3-5%
Increased prevalence since 50s and decreased age of onset: increased stress, decreased social support, more acceptable to report symptoms, overdiagnosis
Gender imbalance: 2:1
Biological Influences
- Genetic: family studies (high rate in relatives of probands), twin studies (higher concordance in identical than in fraternal twins), adoption studies (data is mixed- as should be- environment is important)
- Neurochemistry: low levels of noradrenalin, dopamine, serotonin- no good evidence for mechanism, absolute levels unlikely to be the cause- maybe low density of serotonin receptors- mostly correlational
- Brain structures: amygdala, hippocampus, pre-frontal cortex and anteriour cingulate- don’t know causal relationship
- Neuroendocrine System (hormonal)- overactivity in the HPA axis- regulating response to stress, excess cortisol, damage to hippocampus? lower density of serotonin receptors? early stress linked to depression
Explain Interaction between genetic vulnerability and negative life events as influences on depression
those with 2 short alleles are affected the most by negative life events- 1 short and 1 long deal better, 2 long is best
Psychological Influences
Learned Helplessness Theory- who devised it?
What was his research based on?
Seligman (1967ish)
Animals- dogs- shocks- could stop by pressing lever vs. no control
Attribution Theory (Abramson, Seligman & Teasdale, 1978)
Will attribute negative life events to internal, stable and global things. Will attribute positive life events to external, unstable and specific things.
=Helplessness expectancy- no control
Hopelessness Theory (Abramson, Metalsky & Alloy, 1989)
Helplessness expectancy + negative outcome expectancy (expect bad things to happen)
Schema Theory (Beck, 1976)
Negative schema developed in childhood- cognitive biases in memory, attention, interpretation- magnification, overgeneralisation, arbitrary inference
Depressive Cognitive Triad: negative thoughts about self, world and future
Self-strengthening- taught by parents and these knowledge structures are reinforced because we look for things that are consistent with our schemas- interpretations directed by underlying beliefs
Response style theory (Nolen-Hoeksema, 2002)
Rumination vs distraction, problem solving etc.
rumination stops one from problem solving- women more likely to ruminate, men to distract
Interpersonal approaches
relationships negatively altered by depression:
limited social skills and networks- withdraw and less reactive, no eye-contact, few positive facial expressions
seek excessive reassurance from others
elicit rejection from others
-> maintains or exacerbates depression
Stress-generation hypothesis- self-generated negative life events may partly explain depression recurrence- tendency to think in a certain way can generate more negative life events
When was ECT first introduced and what was it originally used to treat?
1938, Schizophrenia.
Only effective treatment for MD prior to 50s
How many courses are needed of ECT?
How effective is it for severe depression?
Is relapse common?
6-10
85%+
yes
few short-term side effects
What are the 3 waves of drug treatments? 1st
- Monoamine Oxidase Inhibitors (MAOIs)
- 1956- originally used to treat tuberculosis
- takes 14-21 days to take effect
- MAO breaks down serotonin/ norepinephrine
- MAOI block this
- Side effects: hypertension if don’t stick to diet of no tyramine (wine, cheese etc.)
- ideally should only inhibit MAO-A
- still used: parnate and nardil
2nd
- Tricyclic Medications
- 60s- originally to treat psychosis
- takes 14-21 days to take effect
- Block presynaptic reuptake of serotonin and norepinephrine (noradrenaline
- Side effects: anti-cholinergic-dry mouth, blurred vision, tremors, cardiotoxicity
- vegetative symptoms lift first- suicide risk between 10th and 14th days
- still widely used: tofranil, tryptanol
3rd
- Selective Serotonin Reuptake Inhibitors
- 1980s- prozac
- specifically block reuptake of serotonin
- less negative side effects: insomnia, agitation, nausea, sexual dysfunction
- drugs of choice: zoloft, aropax
- possible risk of suicide- esp. in children/adolescents
Is depression caused by low levels of serotonin?
No, we don’t know.
Drug effects non-depressed people too
can be used to treat other things
timing of action not in sync with effect (3-6 weeks for symptoms to lift- possibly slow changes reversing stress-induced hippocampal damage?
What are the top 4 psychological treatments spoken about?
Psychodynamic therapy- some evidence for
CBT- outcomes comparable to drug therapy70-80% get better- lower relapse rates vs. drug treatment alone 29 vs 60%
Interpersonal Psychotherapy- comparable to CBT
Mindfulness-based psychotherapy
What 3 things does IPT target?
Interpersonal/role disputes
Communication analysis, role expectations
Role transitions
Loss of relationship, marriage, job change, illness
Forming new relationships, expanding old ones
Interpersonal deficits
Limited social support network. Social skills training
Does mindfulness target the content of negative thoughts?
No changes relationship with thoughts- deindentification to reduce rumination
Are drugs first choice?
No- no evidence that should be first choice, even for melancholic or ‘biologically’ linked depression
What client characteristics aid recovery through psychological therapies?
Open, less rigid, introspective, conscientious, organised, abstract thinker
What are internalising and externalising disorders?
‘Internalising’ Disorders
◦ Anxiety disorders, Mood disorders
‘Externalising’ Disorders
◦ Oppositional Defiant Disorder (ODD), Conduct Disorder (CD), Attention Deficit Hyperactivity Disorder (ADHD)
Developmental Disorders
◦ Autism, Mental Retardation, Learning Disorders
age epidemiology of MD
Less than 1% in preschoolers ◦ 2-3% in school-age children
Similar rates in both genders
◦ 15-30% in adolescence (age 14-18)
◦ Risk of depression rises greatly in adolescence ◦ Gender ratio 2:1
Dramatic gender differences emerge during early-to-middle adolescence
Why is adolescence a critical time for MD?
negative cognitive styles are consolidated and there are more stressful life events in adolescence- diathesis-stress model
Why is there higher prevalence in females during adolescence?
- more likely to report
- males more likely to self-medicate (alc and drugs)
- hormonal differences- social problems if not hormonally in sync with peers
- higher stress for females: sexual victimisation, body image concerns (80% f vs. 40% m unhappy with bodies), more important for self-esteem- flighting loosing battle-learned helplessness, interpersonal negative events-stress in social networks
- more negative cognitive style in females- ruminate vs. distract (males) or problem solve
Can people under 18 be treated with antidepressants for MD?
No SSRIs only approved to treat OCD in Aus.
Fluoxetine, but none of the other SSRIs, is approved in the US for MDD in young people without a specified lower age limit
Types of prevention for Depression in young people
Prevention (e.g., Gillham, Reivich, Jaycox, & Seligman, 1995)
◦ Uses CBT techniques
◦ universal prevention: given to all students
◦ indicated prevention: aimed at children or adolescents with high scores on symptom scales
◦ selective prevention: target ‘high risk’ groups
◦ young children/toddlers: aimed at parents
Depressed or overprotective parents are treated
