Depression Flashcards
(39 cards)
1
Q
DSM-5 Depressive Disorders
A
- Disruptive Mood Dysregulation Disorder
- Major Depressive Disorder
- Persistent Depressive Disorder (Dysthymia)
- Premenstrual Dysphoric Disorder
2
Q
DSM-IV Mood Disorders
A
DSM-IV Depressive (Unipolar) Disorders
- Major depressive disorder,
- Dysthymic disorder,
DSM-IV Bipolar Disorders
- Bipolar I disorder,
- Bipolar II disorder,
- Cyclothymic disorder
Extremes in normal mood
3
Q
DSM-5 Major Depressive Disorder (MDD)
A
- A single or recurrent depressive episode
- 2 core symptoms:
- Depressed mood most of the day, nearly every day
- Markedly diminished pleasure/interest in activities
4
Q
Differences between DSM-IV and DSM-5
MDD
A
Recurrent thoughts of death, suicide, suicide attempts
- 5 or more is needed, (including 1/ or 2/) in a 2-week period
- There has never been a manic episode or a hypomanic episode.
- symptoms not better accounted for by bereavement: persist longer than 2 months (DSM-IV only)
5
Q
DSM-5 Persistent Depressive Disorder
A
- = DSM-IV Dysthymia
- Depressed mood most of the day, more days than not
- Symptoms are milder, but persist longer than MDD
6
Q
Prevalence of MDD
A
- Lifetime: 16.4%
- One-year in Australia: 3-5% (male-female)
- Steady increase in prevalence since ’50s
- Steady decrease in age of onset
- Reasons:
- Increased speed of change/stress
- Decreased social support/family support
- More acceptable to report symptoms
- Overdiagnosis
- Reasons:
- Gender imbalance (2:1)
- Emerge during adolescence, evens out after 65
7
Q
Biological Influences on MDD
Genetic
A
Genetic:
- Family studies
- High rate in relatives of probands
- Twin studies
- Concordance rates higher in identical twins than in fraternal twins
- Adoption studies
- Data are mixed
8
Q
Biological Influences on MDD
Neurochemistry
A
- Low levels of
- Noradrenalin, Dopamine, Serotorin
- BUT no good evidence for mechanism
- Absolute levels are unlikely to be the cause
9
Q
Biological influences
Brain structures
A
Amygdala, Hippocampus, Prefrontal Cortex, Anterior Cingulate
>> Differences between people with current or history of depression vs no depression
10
Q
Biological Influences
Neuroendocrine system
A
-
Overactivity in the Hypothalamic-pituitary-adrenocortical axis (HPA Stress Axis)
- Involved in regulating response to stress
- Excess cortisol (stress hormone)
- Related to damage to hippocampus?
- Lower density of serotonin receptors?
- Implicates role of (early) stress in depression
- Interaction between genetic vulnerability and negative life events
11
Q
Main changes introduced in DSM-5
A
- Changed DSM-IV Mood Disorders to DSM-5 ‘Depressive disorders’ vs ‘Bipolar and Related Disorders’
- Changed DSM-IV Dysthymia to DSM-5 ‘Persistent Depressive Disorder’
- Removed Grief exclusion from diagnosis of Major Depressive Disorder
- Added ‘Disruptive Mood Dysregulation Disorder’ in DSM-5
- Added ‘Premenstrual Dysphoric Disorder’ in DSM-5
12
Q
Specifier: Melancholic features
MDD
A
- Profound, nearly complete inability to experience pleasure
- Sleep disturbance (e.g. wake up very early in the morning)
- Mood is usually worse in the mornings
- Marked psychomotor retardation or agitation
- Significant anorexia or weight loss
- Excessive guilt
13
Q
Specifier: Catatonic features
MDD
A
- movement disturbance symptoms
- immobility at one extreme
- excessive, purposeless activity at the other extreme
14
Q
Specifier: Peripartum Onset
MDD
A
- Postnatal depression
- Greater among those women experiencing psychosocial stressors
- perceived lack of support from their partner, family and friends
- feeding and physical difficulties with the infant
- stressful life events
- a previous history of depression
- complications during pregnancy
15
Q
Specifier: Seasonal pattern
MDD
A
- Seasonal Affective Disorder
- When there is a regular relationship between the onset of the sufferer’s major depressive episodes and a particular time of the year
- Most often with onset in the autumn or winter months
16
Q
Specifier: Atypical Features
MDD
A
- Mood reactivity (mood brightens in response to actual or potential positive events)
- Weight gain
- Hypersomnia
- Rejection sensitivity
17
Q
Specifier: Psychotic features
MDD
A
- Delusions and/or hallucinations are present
18
Q
Specifier: Anxious Distress
MDD
A
- recognises the strong comorbidity between depression and anxiety
- depression accompanied by significant anxiety
- irrational worry
- inability to relax
- a sense of impending threat
19
Q
Learned Helplessness Theory (Seligman, 1975)
Psychological influences
A
- Lack of control over life events
- Originally an animal model
20
Q
Attribution Theory (Abramson, Seligman , & Teasdale, 1978)
A
- Internal vs external attributions
- Stable vs unstable attributions
- Global vs specific attributions
- Interaction between cognitive style and life event
(Negative events: internal stable and global >> people with helplessness expectancy >> unable to cope when stressful life events occur >> result in depressive symptoms
Positive events: opposite)
21
Q
Hopelessness Theory (Abramson, Metalsky, & Alloy, 1989)
A
- helplessness expectancy plus
- negative outcome expectancy
22
Q
Schema Theory (Beck, 1976)
A
- Pre-existing negative schema
- Developed during childhood (esp if vulnerable)
-
Activated by stress
- Results in cognitive biases (memory, attention, interpretation):
- Arbitrary Inference, Overgeneralization, Magnification
- Depressive Cognitive Triad:
- Negative thoughts about the self, the world, the future become dominant in the consciousness
- Results in cognitive biases (memory, attention, interpretation):
23
Q
Response Style Theory (Nolen-Hoeksema, 2002)
A
Rumination
vs.
Distraction, problem-solving, etc.
24
Q
Interpersonal approaches
Psychological Influences
A
Interpersonal relations are negatively altered as a result of depression
- Depressed people
- have limited social support networks
- seek excessive reassurance from others
- have / display limited social skills
- elicit rejection from others
- >> can maintain or exacerbate depression
25
Interpersonal approaches: **Stress-generation hypothesis**
Psychological Influences
* Stress-generation hypothesis (Hammen, 1991; 2006; Liu, 2013)
* Depressogenic cognitions and behaviours generate negative life events
* Self-generated negative life events may partly explain depression recurrence
26
Biological Treatments: **ECT**
Electroconvulsive Therapy (ECT)
* First introduced in 1938 (to treat schizophrenia.)
* Only effective treatment for MD prior to 1950s
* Applying **brief electrical current to the brain**
* Results in temporary seizures
* A course of 6 to 10 treatments are administered
* **Effective for severe** depression (85%+)
* Still used in people **not responsive to other treatment**
* **Relapse is common**
* Few side effects (short-term memory loss)
* Uncertain why /how ECT works
27
**Monoamine Oxidase Inhibitors (MAOIs)**
Biological Treatments: Drugs
* Introduced in 1956 first MAOI: iproniazide
* **Originally** used to **treat tuberculosis.**
* **Slow** to take effect (14-21 days)
* MAO breaks down monoamines
* Especially serotonin/norepinephrine
* MAO inhibitors block Monoamine Oxidase (A and B)
* **Serious side effect**:
* Can cause ***hypertension*** \>\> ***stroke*** if not on strict diet
* Must avoid Tyramine (beer, red wine, cheeses)
* Ideally MAOI should inhibit MAO-A only
* MAOIs still used: Parnate (tranylcypromine), Nardil (phenelzine)
28
**Tricyclic Medications**
Biological Treatments: Drugs
* Introduced early 1960s: Imipramine
* **Originally** tried to **treat psychosis**.
* Block presynaptic reuptake of Serotonin and Noradrenaline (Norepinephrine)
* **Slow** to take effect (14-21 days)
* Still widely used (Tofranil, Tryptanol)
* **Vegetative symptoms often lift first**
* Have more energy, but mood is not elevated
* ***Increased suicide risk*** between 10th-14th day
* **Negative side effects** are common:
* Anti-cholinergic: dry mouth, blurred vision, tremor
* Cardiotoxicity
29
**Selective Serotonin Reuptake Inhibitors (SSRIs)**
Biological Treatments: Drugs
* Introduced in 1980’s: Fluoxetine (Prozac)
* Drugs of choice at present
* Seltraline (Zoloft), Paroxetine (Aropax)
* Specifically block **reuptake of Serotonin**
* Negative side effects are fewer, less serious
* Insomnia, agitation, nausea, sexual dysfunction
* **Possible risk of suicide,** especially in children/adolescents (Paxil/Aropax)
* **‘off label’ use** has been **common** until recently
* FDA, TGA now r***ecommends warning labels***
30
**Limitations of using medication** to treat depression
* Drug effects also on non-depressed people
* Non-specificity of treatment effects
* Timing of action not in sync with effect
* Uncertain how/why antidepressants work
* Possibly slow changes reversing stress-induced hippocampal damage
31
**Brief Psychodynamic Therapy**
Psychological Treatments
* Some evidence for effectiveness
* Not a recommended first line of treatment
32
**Cognitive Behavioural Therapy**
Psychological Treatments
* **Addresses cognitive errors** in thinking
* NOT positive thinking
* Schema theory (A.T. Beck , A. Ellis)
* Includes behavioural components
* Behavioural activation, Behavioural experiments
* Outcomes are comparable to drug therapy
* **Lower relapse** rates vs drug treatment alone (29% vs 60%)
33
**Interpersonal Psychotherapy (IPT)**
Psychological Treatments
* Beginning / exacerbation of depression:
* Interpersonal/role disputes
* Communication analysis, role expectations
* Role transitions
* Loss of relationship, marriage, job change, illness
* Forming new relationships, expanding old ones
* Address **interpersonal deficits**
* Limited social support network
* Social skills training
* Outcomes are comparable to **CBT**
34
**Drugs** vs. **Psychotherapy**
* Recommendations: drugs as first choice
* no research-based evidence
* Drugs for ‘endogenous/organic/biological’ (melancholic) depression, psychotherapy for ‘reactive’ (non-melancholic) depression
* No good evidence
* Client characteristics for CBT success:
* Introspective, abstract thinker, less rigid, more organised, conscientious
* \>\> not suitable for everyone
* Medication is recommended for patients with severe depression (Because they wouldn't get up and attend therapy)
35
Developmental Psychopathology
**Most common diagnoses**
'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
36
**Epidemiology** of MDD
* \<1% in preschoolers
* 2-3% in school-age children
* No significant gender differences
* 15-30% in adolescence (14-18 yo)
* Risk of depression rises sharply in adolescence
* Significant gender differences emerge
* Gender ratio 2:1
37
Depression in Adolescence
Cognitive diathesis-stress models
* Beck: negative schema
* Seligman: helplessness, negative attributions
* Cognitive style + Negative events =\> Depression
* Predict depression from 12-14 years
Mid-adolescence: critical time for MD
* Negative cognitive styles consolidated
* Increased stress during adolescence
38
What accounts for the **gender differences** in Adolescence Depression?
Possible explanations:
* Reporting differences
* Self-medication in males (head down the road of substance abuse instead)
* Hormonal differences
**Higher stress exposure in females**
* Sexual victimisation (16-19 peak age for rape)
* Body image concerns (80% girls)
* Interpersonal negative events
* ‘Vicarious stress’ in social network
**Higher negative cognitive style in females**
* Different coping responses to stress
* Rumination (females) vs distraction/problem-solving (males, e.g. with drugs)
39
**Causes** of depression in **preadolescents**
* Do children possess negative cognitive styles?
* cognitive diathesis-stress model explains depression from age 12-14
* Negative events =\> cognitive style =\> depression
* Role of **depressed parent(s)**
* genetic vulnerability
* less responsive to children, less contingent to respond, more negative/critical of children
* observational learning (poor coping style, more negative emotion and facial expression, depressogenic thinking etc.)
* Emotional abuse, neglect (more than sexual or physical abuse)
* Secure attachment (protective factor against depression)
