Depressive Disorders Flashcards
What is the common features of DSM-5 Depressive Disorders
- Characterised by sad, empty or irritable mood
- Changes to individual’s capacity to function
- Differ in duration, timing, and/or presumed etiology
Describe DSM-5 Major Depressive Disorder (MDD)
- Made up of Major Depressive Episodes > 2 weeks duration
Not “normal” sadness/grief
A: At least 5 of these symptoms within a 2-week period
1. Depressed mood most of the day, nearly every day (can be irritable mood in children/adolescents)
2. Markedly diminished interest/pleasure in activities, most of the day nearly every day
NEED AT LEAST 1 OF THE FIRST 2 TO CONSIDER A DIAGNOSIS
3. Significant weight loss or gain
4. Insomnia/hypersomnia, nearly every day
5. Psychomotor agitation or retardation, nearly every day
6. Fatigue/loss of energy, nearly very day
7. Feelings of worthlessnes or excessive guilt, nearly every day
8. Diminished ability to think/concentrate/make decisions, nearly every day
9. Recurrent thoughts of death, suicidal ideation, plans or attempts
B: Symptoms cause significant distress or impairment in social/occupational functioning
C: Not attributable to substances or another medical condition
For diagnosis of Major Depressive Disorder (MDD):
- One or more Major Depressive Episodes
- No manic/hypomanic episodes
- Not better explained by a psychotic disorder
Describe the Depressive Disorder Specifiers
What is the Prevalence of MDD and why has this effect come about?
- Anxious distress
- Mixed features (mania- but not enough for diagnosis)
- Melancholic features
- Peripartum onset (postnatal depression)
- Seasonal patern (seasonal affective disorder)
- Catatonia (decreased reactivity to the environment)
- Atypcal features
Prevalence:
Australian National Survey of Mental Health and Wellbeing (2020-21)
- 11.2% lifetime prevalence
- 3-5% one-year prevalence
- Females twice as likely as males to get MDD
- Steady increase of prevalence since the 1950s
- Average age of onset has also decreased
Why Increase?
- Diet
- Lack of physical exercise
- Light/sleep
- Social environment
- Social/economic inequality
- Problematic social media use
- Reduced stigma of diagnosis
COVID-19 resulted in a 28% increase in MDD
- Suspected that this was a temporary increase
- Prevalence of symptoms returned to pre-pandemic levels by end of 2020
- Consistent with research suggesting resilience and recovery is most common response to traumatic events.
Predisposing and Maintaining Factors - Biology & Psychology?
Genetics
Increased risk for first degree relatives
Twin studies estimate 30-50% heritability
Adoption studies
- Data more mixed
Polygenic
Genes x environment (alelle composition)
Chemical imbalance?
Serotonin- no evidence that depression is causd by low levels of serotonin (not a causal relationship), HOWEVER this does not mean antidepressants that act on serotonin are ineffective.
Brain structure changes
- Hippocampus (memory)
- Pre Cortex (executive function, planning, organisation)
- Anterior Cingulate Cortex (attention, motivation, decision-making, social behaviour
- Cause or consequence?
Neuroendocrine (hormonal) system
- Overactivity in HPA axis
- Inolved in regulating response to stress
- Excess cortisol (stress hornome)
- Related to early childhood trauma/adversity
- A potential biological mechanism linking early life stress to depression
Psychology of Depression
Learned helplessness theoy (Seligman, 1975)
- Dogs exposed to unavoidable shock stop trying to escape and show signs of depression
Lack of control over negative life events -> helplessness -> Depression?
But doen’t explain why some people recover and some go on to develop depression?
Attribution theory
Internal vs eternal attributions (it’s me”)
Stable vs unstable attributions (“it’s going to last forever”)
Global vs specific attributions (“it’s going to affect everything I do”)
Helplessness theory
- Stable and global attributions of negative event
- Assuming negative outcomes
- Inferring negative self-characteristics
Cognitive model (Beck, 1976)
- Negatively based thinking is the core process in depression
- Cognitive distortions
- Memory
- Attention
- Interpretation
- Negative Schemas
Response Styles Theory Nolen- Hoeksema, 2002)
- Rumination: Repetitive thinking about the symptoms, causes, meanings, consequences of depression
- Magnifies negative mood
- Interferes with problem solving
- Interferes with goal-directed behaviour
- Impairs concentration
Interpersonal factors
- Interpersonal relationships are negatively altered as a result of depression (Hammen, 2002; Joiner, 1995; Joiner & Metalsky, 2002)
- Limited social support networks
- Excessive reassurance seeking
- Limited ability to display social skills
- Interpersonal difficulties ->maintain or exacerbate depression
- Vicious cycle of depression
What are the treatments for Depression?
Biomedical approaches
Premise that psychological experience stems from biology
- Alter brain functioning to alleviate psychological distress
- Most common approach: psychopharmacology
1. Monoamine Oxidase Inhibitors (MAOIs)
- Introduced in 1956: Iproniazide
- Initially used to treat tuberculosis
- Takes 14-21 days to take effect
- MAO breaks down monoamines (especially serotonin/norepinephrine)
- MAO inhibitors block this process
Serious side effect:
- Ideally MAOI should inhibit MAO-A only, but also block MAO-B
- Can cause hypertension -> stroke
- Must avoid Tyramine (beer, red wine, cheeses)
- MAOIs still used: Parnate (tranylcypromine), Nardil (phenelzine)
Tricyclic Medications
Introduced early 1960s: imiparamine
- Originally used to treat psychosis
Blocks presynaptic reuptake of serotonin and noradrenaline (norepinephrine)
- 14-21 days to take effect
- Still widely used
- Increased suicide risk between 10th-14th day
- Vegatative symptoms often lift first (increased energy)
Nwgative side effects are common:
- Anti-choligernic: dry mouth, blured vision, tremor
- Cardiotoxicity
Selecive Serotonin Reuptake Inhibitors (SSRIs)
- Introuced in 1980’s: fluoxetine (Prozac)
- Most commonly prescribed in Australia
- Escitolopram (Lexapro), sertraline (Zoloft)
Blocks reuptake of serotonin
- Negatve side effects are fewere, less serious
- Insomnia, agitation, nausea, sexual dysfunction (norgasmia)
- Serotonin and norepinephrine reuptake inhibitors (SNRIs)
- Duloxetine (Cymbalta), venlafaxine (Effexor)
- Noreprineprhine and dopamine reuptake inhibitors (NDRIs) buproprion (Wellbutrin)
How do SSRIs work?
SSRI blocks reabsorpion of serotonin
- Increases availability in the synapse
- No good evidence of an abormality of serotonin in people who are depressed
- SSRIs are effective
How do SSRIs improve depression?
Neurogenesis hypothesis
- Chronic stress alters neuronal circuits in the brain
- Stress decreases formation of new neurons in brain
- Antidepressants can enhance synaptic plasticity
- This takes time, accounting for delay betwen starting antidepressants and their effects
Negative bias hypothesis
- Negative bias in thoughts, feelings, and beliefs thought to maintain depression
Antidepressants can increase the relative processing of positive information through changes in parts of the brain that control emotional processing
- Over time, this could reduce depression symptoms
Are psychedelics the future?
- Psilocybin recently approved in Australia for treatment of severe depression (in combination with psychological treatment)
- Large effect sizes, but more research needed with larger samples + placebo controls
Electroconvulsive Therapy (ECT)
- Applying brief electrical current to the brain
- Results in temporary seizures
- Effectiv for severe depression (85%+)
- Still used in treatment-resistant depression
- Few side effects (short-term memory loss)
- Relapse is common
Cognitive Behavioural Therapy (CBT)
- Based on the cognitive model (Beck, 1964; Ellis, 1962)
- Thoughts/interretations of events determine how peoplefeel about those events
- Addresses cognitive biases in thinking
- Cognitive restruturing
- Behavioural experiments
- Behavioural activation
- Outcoes are comparable to drug therapy
- Lower relapse rates vs drug treatment alone (meta-analysis: 29 vs 60%)
CBT based on a formulation of the clients current problems
Predisposing -> Precipitating -> Perpetuating -> Presenting problem
Then
Prescrbe Treatment -> Plot Progress and Pattern of Response -> Prevent relapse
Interpersonal Psychotherapy (IPT)
Focuses on interpersonal relationships contributing to depression
- Interpersonal/role disputes
- Role transitions
- Interpersonal deficits
Mindfulness-based Cognitive Therapy (MBCT)
- Mindfulness: intentional, nonjudgemental attention to the present moment
- Notice and distance from depressive thoughts
- Mechanism: reduces rumination
- Was specifically developed to reduce relapse
- As effective as prophylactic treatment with maintenance antidepressant medication (Piet & Hougaard, 2011)
Acceptance and Commitment Therapy (ACT)
- Acceptance of problematic thoughts/emotions/sensations/images
- No longer see them as symptoms, but harmless psychological events
- Aims to move towards a more valued and fulfilling life
What are the treatment recommendations according to the Royal Australian and New Zealand College of Psychiatrists (RANCP) clinical practice guidelines for mood disorders?
Biopsychosocial lifestlye approach and provide the following specific clinical recommendations:
- Alongside or before prescribing any form of treatment, consideration should be given to the implementation of strategies to manage stress, ensure appropriate sleep hygiene and enable uptake of healthy lifstyle changes
- For mild to moderate depression, psychological management alone is an appropriate first line treatment, especially early in the course of illness.
- For moderate to severe depression, pharmacological management is usually necessary and is recommended first line, ideally in conjunction with psychosocial interventions.
