AQA Psychopathology - OCD

List two behavioural characteristics of OCD
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List two behavioural characteristics of OCD
-Compulsions that are repetitive and reduce anxiety caused by obsessions, e.g. hand washing, checking locks.
-Avoidance of anxiety triggering situations, e.g. taking out the rubbish if you obsess over germs
List three emotional characteristics of OCD
-anxiety and distress from obsessive thoughts
-accompanying depression
-guilt and disgust, often directed at self or at an external obsession
List three cognitive characteristics of OCD
-obsessive thoughts that are recurring, e.g. everything is contaminated by germs
-cognitive coping strategies such as excessive prayer and meditation
-awareness of irrationality of obsessions
What are the two biological explanations of OCD?
Genetic and neural explanations
What did Lewis find from studying his OCD patients and when was this conducted?
Conducted in 1936
37% of his OCD patients had parents with OCD, and 27% had siblings
What causes genetic vulnerability to OCD? Give an example of this
Candidate genes that are passed between generations (according to the genetic ex0anation)
E.g. 5-HT1D beta, involved in serotonin regulation
Define diathesis-stress model
a diagnostic model that proposes that a disorder (OCD) may develop when an underlying genetic vulnerability is coupled with a precipitating event (environmental factors)
OCD is believed to be caused by different combinations of candidate genes in different people: this means OCD is what?
Aetiologically heterogenous / polygenetic
What evidence for the genetic evidence of OCD was presented through twin studies? What is a limitation of this?
Nestadt 2010
68% monozygotic twins both diagnosed with OCD and 31% dizygotic twins
Whilst this provides evidence that genes play a role, it also indicates that they cannot be the only factor as monozygotic twins share 100% of their DNA, hence if this was the only factor the concordance rate would be 100%; this does however support the diathesis stress model as it could be that an environmental factor is required also.
What did Cromer et al find and when?
2007
Over half of his OCD patients had experienced a traumatic event, indicative of the vitality of environmental factors but also meaning that genes are not solely the cause of OCD. Likely that both play a role as some patients had OCD without a traumatic event also
Why is the usefulness of the genetic explanation limited?There are potentially thousands of candidate genes due to OCD being aetiologically heterogenous, ergo finding a definitive cause and ergo cure is unlikelyDescribe serotonin as a neural explanation of OCDLow levels of serotonin leads to impaired transmission of mood related information, leading to a lowered mood and linked to the obsessive thoughts characterising OCDWhat area of the brain functioning abnormally leads to impaired decision making and OCD symptoms?Abnormal functioning of the frontal lobeWhat area of the brain functioning abnormally leads to greater processing of negative emotions?Abnormal functioning of the parahippocampal gyrusWhat is the supporting evidence for the role of serotonin as a cause of OCD?Antidepressant studies - increased levels of serotonin reduce OCD symptoms, suggesting it's related to its onset and developmentWhy is the idea of OCD's comorbidity with depression a limiting factor?As depression is also linked to low levels of serotonin, meaning the OCD-serotonin link is not unique and that the low levels of serotonin seen in patients may be due to accompanying depression and not OCDWhy is the cause-effect relationship between serotonin and OCD not known?It is unclear whether low levels of serotonin cause OCD or whether it's the other way around, weakening the neural explanation.What is the purpose of drug therapies to treat OCD?To increase the levels of a specific neurotransmitter (serotonin, noradrenaline) in the brain, which in turn increases the stimulation of the post synaptic neuron.What does SSRI stand for?selective serotonin reuptake inhibitorDescribe the action of SSRI's-as serotonin is released by the presynaptic neuron, it travel across a synapse as it chemically conveys the mood related information/ action potential to the post synaptic neuron, where it is then reabsorbed by the presynaptic neuron to be reused or broken down -SSRI's prevent the reabsorption and breakdown of serotonin, increasing its levels in the synapse and causing it to continue stimulating the postsynaptic neuron to compensate for its low levels.What is the benefit of using SSRI's in combination with CBT?There is a decrease in emotional symptoms which allows the individual to engage more actively with the CBTWhat is the dosage of Fluoxetine (SSRI)?20mg per day, can be increased gradually. Around 3-4 months to see major improvementName the older antidepressant that has more side effects than SSRI's and give an exampleTricyclics e.g. clomipramineWhat are SNRI's and when are they used?Serotonin-noradrenaline reputable inhibitor Same action as SSRI's but with both serotonin and noradrenaline Used in those who do not respond to SSRI'sGive evidence of the effectiveness of SSRI'sSoomro et al 2009 found SSRI's saw better results than the control placebo group, proving their effectivenessLimitation of the effectiveness of SRRIs as a treatment for OCDSkapinakis et al. 2016 - argued cognitive and behavioural therapies work better than antidepressants for OCDWhy is the non-disruptive and cost effective nature of drug therapies a benefit?1. Doesn't interfere with the life of the patient - saves them time. 2. Costs less than psychological treatments therefore it is good value for public health systemsWhy can't we trust the evidence of the effectiveness of SSRIs?Effectiveness of SSRI's is biased because drug companies suppress evidence (don't publish) that doesn't support their effectivenessAs with any medication, what is a major limitation of antidepressants?Side effects, e.g. indigestion, loss of sex drive, blurred vision.