Depression Flashcards
1
Q
DSM-5
A
Symptoms:
- emotion - depressed mood or a loss of interest or pleasure
- motivation - less interest or enjoyment of activities
- physical - insomnia/excessive sleep (may sleep at strange times of the day= isolating, significant weight change (5%)
- behavioural - increase/reduction in physical movement (psychomotor agitation/ retardation), substantial fatigue or a loss of energy
- cognitive - worthlessness, guilt, lack of concentration or ability to think and make decisions
- usually more friends and family realise then themselves
- cause significant impairment in social or occupational functioning
- some medication can induce depression - symptoms are not due to direct physiological effect of a substance e.g. drug, or a general medical condition
- have negative thoughts about self and future
- poor concentration and thinking and decision making (self fulfilling prophecy) can feed into negative thoughts
- some conditions may mimic a coexist with major depressive disorder e.g. substance abuse, medical illess, other psychiatric disorders and bereavement
2
Q
Who develops depression?
A
- 2-5% anual prevelance
- lifetime prevalence between 6-25%
- 2:1 women to men (Hilt et al., 2009)
- low social status and unemployed people more than high SES
- difficultly with prevalence studies - Crossnational Collaborative Group (1996) - use a different diagnostic criteria across studies, so hard to compare. Social stigma many years ago, so some people may not report it, and there are differences between Western and non-Western countries
3
Q
Course
A
- 80% have recurring episodes, most episodes improve after 4-6 months, even if untreated
- relapse typically in 5 years, but each relapse time lengthens and episodes shorten
- as go on, a reduction in the amount of stress needed to trigger the episode
4
Q
Consequences
A
- mild = missed work, bad social functioning
- moderate-severe = interferes with work and relationships
- severe = big impact, something easy becomes hard, many spend ages in bed
5
Q
Comorbidity
A
- 59% anxiety, 24% substance abuse
- personality disorder - 50-85% inpatients and 20-50% outpatients
6
Q
Monoamine theory
A
- monoamine is a generic term for noradrenaline (NA), serotonin (5-HT) and dopamine (DA)
- neurotransmitters are chemicals that help communication of impulses
- neurotransmitters are stored in vesicles and released and bind to receptors
- if the reuptake of monoamines is too quick, then there is a low amount in the synapse
- depression is caused by low levels of NA and/or 5-HT
- very low 5HT in suicidal’s - post mortem (cause and effect)
7
Q
Vetulani and Nelapa (2000)
A
- moonoamine oxidase inhibitors (MAOI) blocks the degrading enzyme MAO (prevents the breakdown of neurotransmitter). Therefore, more are in the brain
- tricyclic antidepressants (TCA) - block reuptake, fit into vesicles. Both increase monoamine levels in the synapse
8
Q
Problems with antidepressant drugs
A
- need to develop new as: there are lots of side effects, potentially could overdose (addictive)
- 30% of patients had no effect
9
Q
Harmer (2009)
A
- therapeutic delay - 3-4 weeks, immediate impact on neurotransmitters, but no physical improvement for a while. Works similar to cognitive therapies
- reuptake inhibition is immediate, but the response is delayed - if receptors are blocked, then negative feedback causes receptors to down regulate, which changes the firing patterns, so releases more serotonin. When you have lower levels of serotonin, receptors are very sensitive to transmit, so she drugs make more neurotransmitters, receptors get rid of them. Therefore, receptors tend to get desensitised, which takes 3-4 weeks
10
Q
Arroll et al (2005)
A
- 55-65% show improvement rates, although relapse rates are common
11
Q
Mutlow et al (1998)
A
- more effective than placebos
- second generations are not lethal if you overdose in most cases
- fewer side effects
- can have nausea in the first 4-6 days of treatment, preventing further usage
- relapse 40-50%
12
Q
Kirsch (2010)
A
- do antidepressants really work?
- only really work for severe depression
- most/ all benefits due to the placebo effect
- popular antidepressants may induce a biological vulnerability, making people more likely to be depressed in the future
- not clinically significant, only statistically significant
13
Q
Ilyars and Moncrieff
A
- linear regression
- prescriptons for drug use increased by 6.8% per year, in line with the average
- antidepressants increased by 10%, may be explained by longer treatment, but should also receive psychological treatment after 28 days, however, number of meds required is still increasing
- possibly patient choice
14
Q
Beck (1967, 1987)
A
- early experiences e.g. early adversity, or abusive parenting may lead to an individual forming negative schemas about themselves, which may lower their self belief
- schema content may be global (I am a bad person), or conditional (I must be productive or life has no purpose).
- we all develop schemas, but some may lay dormant, or influence how we see the world
- maintenance cycle - schemas give rise to: negative automatic thoughts, cognitive bias, and a negative cognitive triad
- onset of life events e.g. loss and reactive negative cognitive schematise and assumptions
- may be a physical loss, or loss of a social role
15
Q
Epp et al (2012)
A
- attentional bias
- emotional stroop task in depression
- pps slower to say colour of depressing word - more cognitive interference
