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psychopathology (depression (characteristics (emotional: low mood, anger,…
psychopathology
depression
characteristics
emotional: low mood, anger, lowered self-esteem
cognitive: poor concentration, attending to and dwelling on the negative, absolutist thinking- "black and white thinking"
behavioural: activity levels reduced, disruption to eating and sleeping, aggression and self harm
cognitive-explanation
Beck says depressed people have acquired a negative schema therefore adopt a negative view of the world this leads to systematic cognitive biases in thinking. The negative triad: -'ve view of the SELF, WORLD and FUTURE
Ellis ABC model: A-activating event B-belief (rational or irrational) C- consequence irrational-healthy emotions irrational-unhealthy the source of irrational thoughts lies in masturbatory thinking- certain ideas must be true in order to be happy.
evaluation
strength: 1)there is research supporting the link between depression and irrational thoughts by Hammen and Krantz- depressed participants made more errors in logic when asked to interpret written material in comparison to non-depressed.
HOWEVER, doesn't mean that negative thoughts are the cause of depression 2) practical application to therapy (CBT)- found to be the best treatment for depression
limitation: 1)cognitive approach blames the client rather than situational factors for their disorder 2) irrational beliefs may be realistic normal people have rose tinted view depressed people don't
cognitive-treating
Ellis-REBT (rational emotive behaviour therapy)makes it ABCDEF- D- disputing irrational thoughts E- effecrs of disputing F- feelings that are produced break link between negative life event and irrational thought 2 types of disputing- 1) empirical disputing whethere there's actual evidence to support the negative belief 2) logical argument- does the negative thought logically follow the facts
CBT: (Beck's)-identify automatic thoughts about the self, worl and future and challenge them. they test the reality of negative believs by goving them homework- (BEHAVIOURAL ACTIVATION- make them go do certain activities part of therapy)
evaluation
strength: Ellis there's a 90% success rate however says not always effective as patients don't put their revise beliefs into actions
limitation: lack of success due to suitability and individual differences therapy doesn't work on people with high levels of stress or irrational beliefs
phobias
characteristics
behavioural:panic, avoidance,endurance- opposite to avoidance remain with stimuli and experience high level of anxiety
cognitive: selective attention to the phobic stimulus (keep looking at it!), irrational beliefs, cogitive distortions(brain distorts images that look normal to others e.g snakes)
emotional: Phobias are classed as anxiety disorders, emotional responses are unreasonable
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OCD
characteristics
emotional: anxiety and distress, accompanying depression, guilt and disgust.
behavioural: avoidance, compulsions 1)repetitive-tend to repat a behaviour e.g hand-washing 2) they reduce anxiety- no obsessions just irrational anxiety.
cognitive: obsessive thoughts, cognitive strategies to deal with obsessions (adopt these to help with daily life), insight into excessive anxiety(they know its irrational this is needed to diagnose a person with OCD if they didnt have it they would have a different mental disorder)
biological-explanation
Genes are involved in individual vulnerability to OCD. This suggests that OCD runs in families although what is probably passed on from one generation to the next is genetic vulnerability not the certainty of OCD
One genetic explanation is genetic diathesis-stress which suggests that the individual gene is the one that creates vulnerability. environment stress needed to trigger condition
genes which create vulnerability for OCD called candidate genes. These genes are mostly used for the regulation of the development of serotonin system. e.g the 5HT1-D beta is used for the transportation of serotonin across synapses. This gene also causes lower levels of serotonin which is associated with OCD.
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COMT regulates the production of the neurotransmitter dopamine. there is another form of this gene commonly is OCD patients causing lower levels of the COMT gene and higher levels of dopamine
neural explanations suggest that abnormal levels of neurotransmitters, in particular serotonin and dopamine, are implicated in OCD. Dopamine levels are usually high in OCD patients. On the other hand it is lower levels of serotonin that is associated with OCD. This conclusion is based on the fact that antidepressant drugs that increase serotonin activity have been shown to reduce OCD symptoms.Also several areas of the frontal lobe of the brain are thought to be abnormal with people who have OCD. Their caudate nucleus normally suppresses signals from the orbitofrontal cortex. In pet scans it showed that whilst the symptoms of OCD are active there is heightened activity in the OFC.
evaluation
strength: evidence to support the claims. The evidence for the genetic basis of OCD comes from the studies of first relatives (parents or siblings )and twin studies. Nesadt et al identifies 80 patients with OCD nnd 334 first relatives and compared them with 73 controlled patients without mental illnesses and 300 of their relatives. They found that people with a first degree relative with OCD are 5x greater risk of having the illness themselves at some time in their life. However these concordance rate are never 100% which means environmental factors do come into play
limitation: there's the claim that there is no specific gene unique to OCD but they are predisposed factors towards it. Paul and Leckman studied patients with Tourettes and found that they both have one gene t that is the samee that determines both . This is also found in children with autism, anorexia or bulimia. This battles the claim that there are different genes like SERT or COMT that can be indicators for OCD.
treating
SSRIs are one type of antidepressant drug,e.g Prozac. When serotonin is released from the presynaptic cell into the synapse, it travels to the receptor sites on the postsynaptic neuron. Serotonin which is not absorbed into the postsynaptic neuron is reabsorbed into the sending cell. SSRIs increase the level of serotonin available in the synapse by preventing it from being reabsorbed into the sending cell. This increases the level of serotonin in the synapse and results in more serotonin being received by the receiving cell. Antidepressants improve mood and reduce anxiety which is experienced by patients with OCD.
BZs are a range of anti-anxiety drugs. BZs work by enhancing the action of the neurotransmitter GABA. BZs have a general quietening influence on the brain and consequently reduce anxiety, which is experienced as a result of the obsessive thoughts. It does this by reacting with special sites on the outside of the receiving neuron. Chlorine ions make it harder for the neurons to be stimulated by other neurotransmitters thus slowing down its activity and making the person feel more relaxed.
evaluation
strength:Typically a randomised control trial is used to compare the effectiveness of the drug in comparison to a placebo. Soornro et al reviewed 17 studies of the use of SSRIs with OCD patients and found them to be more effective than placebos in reducing the symptoms of OCD up to three months after treatment this is only in the short term. However one of the issues regarding the evaluation of the treatment is that most studies are only 3 to 4 months duration, and therefore little long term dasta exists(researched by Koren et al).
limitation:all drugs have side effects like nausea or headaches which are common for SSRIs. These can make the patient prefer not to take the drug, tricyclic antidepressant tends to have more side effects as a result tricycles are used only when SSRIs aren't effective. Ashton also researched BZs and found they increase aggressiveness and long term impairment with memory. There are also problems with addiction as a result the treatment should be limited to a maximum of 4 weeks.