Psychopathology - 05 The Biological Approach To Explaining and Treating OCD Flashcards

1
Q

What two factors of the biological approach can be used to explain the causes of OCD?

A

1)genetic explanations
2)neural explanations

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2
Q

What do genetic explanations suggest about the cause of OCD?

A

suggests that individuals inherit specific genes from their parents that are related to the onset of OCD

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3
Q

What evidence did Lewis (1936) have which suggested that OCD is inherited?

A

-37% of his patients with OCD had a parent with OCD
-21% had siblings with OCD
-suggesting that genes play a role

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4
Q

What evidence did Nestadt et al (2010) have to suggest that OCD has genetic links?

A

-concordance rate of 68% for monozygotic twins and 31% for dizygotic twins
-suggests strong genetic component

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5
Q

What are the two genes which have been identified as having a link to OCD?

A

1)COMT gene
2)SERT gene

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6
Q

How does the COMT gene link to OCD?

A

-regulates the production of dopamine
-COMT gene has mutated causing high levels of dopamine

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7
Q

What did Tukle et al (2013) find about the COMT gene and OCD?

A

-compared 101 OCD sufferers with 100 healthy controls
-found lower activity of COMT gene resulting in higher levels of dopamine

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8
Q

How does the SERT gene link to OCD?

A

-affects the transport of serotonin
-SERT gene has mutated causing low levels of serotonin

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9
Q

What did Ozaki et al find about the SERT gene and OCD?

A

-found mutated SERT gene in two different families
-6/7 family members had OCD

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10
Q

What does polygenic mean?

A

something is not caused by a single gene but that many genes are involved

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11
Q

How many genes did Taylor say may be involved in OCD?

A

230 genes

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12
Q

weakness of genetic explanations of OCD (not the sole cause of OCD)

A

-Lewis only 37% had OCD parent and Nestadt concordance rate 68% in MZ twins
-suggests must be another reason for OCD
-if genes was sole reason concordance rate would be 100% and all patients would have OCD parent too

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13
Q

weakness of genetic explanations of OCD (deterministic)

A

-suggests no free will or control as it is determined through genes
-problem as patients may become passive and do nothing to help

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14
Q

weakness of genetic explanations of OCD (environmental factors ignored)

A

-environment can trigger/increase risk of OCD
-Cromer et al (2007) 1/2 OCD patients had traumatic events in past and OCD was more severe with more than 1 trauma
-so cannot be entirely genetic

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15
Q

weakness of genetic explanations of OCD (need for interactionist approach)

A

-needs diathesis-stress model
-individual may have a genetic vulnerability to develop OCD
-BUT it is the interaction between genes and environment that causes OCD

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16
Q

What are the two neural explanations of OCD?

A

1)neurotransmitters
2)abnormal brain circuits

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17
Q

What are the 2 neurotransmitters which are thought to link to OCD?

A

1)dopamine
2)serotonin

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18
Q

How does abnormal levels of dopamine link to OCD?

A

-dopamine levels are high in people with OCD

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19
Q

What evidence is there to suggest that high levels of dopamine cause OCD?

A

-animal studies
-high dosages of drugs which enhance levels of dopamine induce stereotyped movements resembling the compulsive behaviour of OCD

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20
Q

How does abnormal levels of serotonin link to OCD?

A

-lower levels of serotonin are associated with OCD

21
Q

What evidence is there to suggest that low levels of serotonin cause OCD?

A

-antidepressant drugs that increase serotonin activity have been shown to reduce OCD symptoms

22
Q

What symptom of OCD is serotonin thought to cause?

A

obsessive thoughts

23
Q

What is low levels of serotonin likely due to?

A

serotonin being removed too quickly from the synapse (reuptake) before it is able to transmit its signal

24
Q

What abnormal brain circuit is linked to people with OCD?

A

the worry circuit

25
Q

What happens at the first stage of the worry circuit?

A

the Orbital frontal cortex (OFC) notices when something is wrong and it sends a worry signal to the Thalamus

26
Q

What happens at the second stage of the worry circuit?

A

Caudate nucleus usually supresses the worry signal and stops it from reaching the Thalamus BUT in OCD patients it is damaged

27
Q

What happens in the third stage of the worry circuit?

A

Caudate nucleus fails to supress the worry signal and so the Thalamus is alerted

28
Q

What happens in the forth stage of the worry circuit?

A

Thalamus sends a signal back to the OFC which responds by increasing compulsive behaviours and anxiety

29
Q

What did Cormer say about the role of serotonin in the worry circuit?

A

-serotonin plays a key role in the operation of the worry circuit and the caudate nucleus
-so abnormal serotonin levels might cause these areas to malfunction

30
Q

Supporting evidence for the role of neural mechanisms in OCD + counterargument

A

-antidepressants like SSRIs work on the serotonin system, increasing the levels
-they are effective in reducing symptoms suggesting that serotonin systems are involved in OCD
-BUT not all sufferers respond to antidepressants suggesting that it is not the neural network causing OCD in these patients

31
Q

weakness of of neural explanations (cause of effect?)

A

-neural mechanisms may not cause OCD
-could be a result of OCD rather than the cause itself
-problem as if neural mechanisms are not the cause then we need to find out what is
-also if neural mechanisms do not cause OCD, no point using antidepressants to treat it

32
Q

What do biological treatments for OCD aim to do?

A

restore chemical imbalances in the brain since this is assumed to be the main cause of the disorder

33
Q

What are the two types of drugs used to treat OCD?

A

1)antidepressants
2)anti-anxiety drugs

34
Q

What re the three types of antidepressant drugs used to treat OCD?

A

1)SSRIs (selective serotonin reuptake inhibitors)
2)TCAs (tricyclics)
3)SNRIs (serotonin-noradrenaline reuptake inhibitors)

35
Q

Which antidepressant is the most common used to treat OCD?

A

SSRIs

36
Q

How do SSRIs work?

A

-increase serotonin available in synapse by preventing reabsorption
-this increases serotonin in synapse which improves serotonin concentration at receptor sites on post-synaptic neuron
-this increases stimulation on receiving nerve

37
Q

How do TCAs work?

A

-block transporter mechanism that reabsorbs serotonin and noradrenaline in pre-synaptic cell after firing
-so more is left in synapse, prolonging activity
-only used when SSRIs are ineffective

38
Q

How do SNRIs work?

A

-increase serotonin and noradrenaline
-only used when SSRIs are ineffective

39
Q

What anti-anxiety drug is used to treat OCD?

A

benzodiazepines (BZs)

40
Q

What are two example of BZ drugs?

A

Valium and diazepam

41
Q

What do BZ drugs aim to do?

A

reduce anxiety which will reduce compulsions

42
Q

How do BZs work?

A

-enhance action of GABA (gamma-aminobutyric acid)
-GABA tells neurons in brain to slow-down and stop firing
-around 40% of neurons respond
-means the drugs have quietening influence on brain reducing anxiety, experienced as a result of obsessive thoughts

43
Q

Effectiveness of drug treatment for OCD

A

-Soomro et al (2008) reviewed 17 studies of SSRIs found them to be more effective than placebos in reducing symptoms for up to 3 months
-BUT most studies only last 3 months so little long term data exists

44
Q

Suitability of drug treatment for OCD

A

do not work in all OCD patients so not suitable for all patients

45
Q

Conflicting evidence of drug treatment for OCD

A

-unreliable evidence, some psychologists believe evidence favouring drug therapy is biased as it is sponsored by drug companies
-only publish studies which show their drug as being effective (publication bias)

-Simpson, 45% cases relapsed in 12 weeks , compare to only 12% who had CBT

46
Q

Alternative treatments of drug treatment for OCD

A

-drugs criticised for treating symptoms not the cause
-plus once a patient stops taking drugs they are prone to relapse
-so CBT may be more effective long-term solution to provide a lasting treatment and a potential cure

47
Q

Practical issues of drug treatment for OCD

A

-cost effective, beneficial to health providers plus CBT needs patients to be motivated to engage whereas drugs are non-disruptive

-side effects BZs only recommended for up to 4 weeks also diminishes effectiveness as patients will often stop taking it if they experience negative side effects

48
Q

ethical issues of drug treatment for OCD

A

-side effects e.g. nausea, headaches and insomnia & BZs also highly addictive
-valid consent, people often in vulnerable state and so may not fully understand things e.g. side effects & fact it is short term solution
-so patient may not be making full decision