OCD Flashcards

1
Q

What are obsessions

A

Persistent, intrusive, recurring thoughts or images

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2
Q

What are compulsions

A

Repetitive, ritualistic behaviour

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3
Q

What is the OCD cycle

A

A cycle used to explain how OCD occurs which consists of obsessions leading to anxiety which causes an individual to undergo compulsions leading to temporary relief

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4
Q

What is the genetic explanation of OCD

A
  • OCD tends to run in families
  • Twin studies are used to see how a trait can be inherited and to see the concordance of the trait
  • Studies have been done such as comparing genetic material from an OCD sufferer and a non-OCD sufferer
  • This suggests that there are particular genes that make someone more likely to suffer from OCD
  • Diathesis stress model suggests some genes leave people more likely to suffer from OCD
  • The specific genes that have been implicated to OCD are:
  • The COMT gene- helps to reduce the action of dopamine. The variation in the COMT gene decreases the amount of COMT available and therefore dopamine is not controlled and there is probably too much dopamine(associated with OCD but also with many other psychiatric disorders)

The SERT Gene- This affects the transport of serotonin, creating lower levels of this neurotransmitter. Lower levels of serotonin have been implicated with OCD

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5
Q

What is the brain structure explanation to OCD

A

Some biopsychologists believe that OCD is caused by brain abnormalities

The worry circuit:

  • The OFC, sends signals to the thalamus via the caudate nucleus about things that are worrying, such as a potential germ hazard
  • To get to the caudate nucleus, the cingulate cortex acts as a relay system between the two. It is involved in emotions also
  • The caudate nucleus usually supresses/regulates signals from the OFC
  • When the caudate nucleus is damaged, it fails to suppress minor ‘worry’ signals and the thalamus is alerted, which sends signals back to the OFC and confirms the worry

This increases compulsions and anxiety

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6
Q

What is the neurotransmitter explanation to OCD

A
  • Serotonin is a neurotransmitter linked to OCD. It sends mood-relevant information. If this does not take place, then mood and mental processes can be affected

Serotonin

  • Low levels of serotonin have been found in people with OCD(Hu, 2006)
  • Serotonin is said to play a very active role in the orbital-frontal cortex and the caudate nucleus
  • It may well be that these low serotonin levels lead to abnormal functioning of the brain involved in OCD(OFC and caudate nucleus)

Use of drugs called SSRI’s has shown a reduction in OCD symptoms which suggests that there is a link between serotonin levels and OCD.

SSRI’s block neurotransmitters from reattaching to the vesicles in order to increase the chance of binding onto the other neuron in order to increase the likelihood of the other neuron generating it’s own electrical impulse

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7
Q

AO3 of genetic explanation of OCD

A

There are ethical issues such as in twin studies it is ethically wrong to separate twins at birth. It also does not take into account the environment(nurture) therefore it may be seen as deterministic and not taking into account the cognitive approach

It cannot be 100% inherited because 100% concordance rate would suggest completely identical traits and therefore it suggests OCD cannot be 100% genetic and OCD is also caused by environmental stress

It can be seen as problematic because it suggests that because OCD is polygenic, there is not 1 drug that can treat OCD which therefore makes biological treatment for OCD a lot more challenging

The small sample size reduces the reliability of the biological explanation because it means it cannot be generalised to all twins

There is strong evidence for the idea that genetic variation can make a person more or less vulnerable to OCD. However, OCD does not appear to be entirely genetic in origin and it seems that environmental risk factors can also trigger or increase the risk of developing OCD. In one study for example, Kiara Cromer et al.(2007) found that over half the OCD clients in their sample had experienced a traumatic event in their past. OCD was also more severe in those with one or more traumas. This means that genetic vulnerability only provides a partial explanation for OCD

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8
Q

AO3 of neurotransmitters explanation of OCD

A

40% of OCD patients do not respond to SSRI treatment. This may suggest that low serotonin is not the only cause of OCD and that there may be other neurotransmitters that can cause OCD

The limitation of the neurotransmitter explanation of OCD is that OCD usually links to people experiencing clinical depression as well. This depression could then involve disruption to the action of serotonin. This could then be a limitation serotonin activity is disrupted in many people with OCD because they are depressed as well and so serotonin may not be relevant to OCD symptoms

Being reductionist can be useful as it allows researcher to have a precise focus when investigating a disorder and this allows them to break it down into smaller parts that are easier to investigate. This allows researchers to focus on a specific problem and come to a conclusion. The limitation is that it can it can oversimplify the human behaviour, neglecting the complexities of the mind and not fully understanding the cause of the disorder.

The cause and effect argument is when the cause states why something happens. An effect states a result or outcome. This applies to neural explanations as for example it is suggested that abnormal levels of neurotransmitters, in particular serotonin and dopamine, cause OCD.

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9
Q

AO3 of Brain Abnormalities explanation of OCD

A

Treating parts of the brain involved with OCD through neurosurgery tends to show an improvement in OCD symptoms-Neurosurgery targets specific areas of the brain associated with OCD, such as the orbitofrontal cortex, anterior cingulate cortex, and caudate nucleus. Improvement in symptoms following surgery suggests that these brain regions play a crucial role in the disorder.

There is evidence to show that some neural system (e.g. serotonin) do not work normally in people with OCD. According to the biological model of mental disorder this is most easily explained by brain dysfunction causing the OCD.
However, this is simply a correlation between neural abnormality and OCD, and such correlations do not necessarily indicate a causal relationship. It is quite possible that the OCD (and its accompanying depression) causes the abnormal brain function or both are influenced by a third factor.

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10
Q

What are the 3 main methods of treating OCD(Biological)

A

Antidepressants, Tricyclics/SNRI’s, Benzodiazepines

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11
Q

How do antidepressants

A
  • Raise serotonin levels
  • This is done by blocking its reuptake from the synapse back into the releasing neuron
  • This results in serotonin for a longer period of time
  • This may take up to 12 weeks or might not take effect
    SNRI’s and Tricyclics and BZs
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12
Q

How do Tricyclics/SNRI’s work

A
  • Inhibits serotonin and norepinephrine reuptake within the presynaptic terminals
  • This results in elevated concentrations of the neurotransmitters within the synaptic cleft
  • The increased levels of serotonin and norepinephrine in the synapse can contribute to the antidepressant effect.

These drugs tend to have more side effects then SSRI’s so are only used if SSRI’s are not working

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13
Q

How do Benzodiazepines work

A
  • Anti-anxiety drug
  • They work by increasing the action of the neurotransmitter called GABA.
  • GABA is an inhibitory neurotransmitter. This means it makes the receiving neurone less likely to fire which effectively ‘slows down’ the brain
  • Helps worry circuit

As a result of this, anxiety is reduced

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14
Q

What is the cognitive therapy called that can help treat OCD

A

CBT(Cognitive behavioural therapy)

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15
Q

Key Characteristics of CBT

A

Goal orientated

Runs for around 3 months

Two components- cognitive (which focuses on changing thought processes) and behavioural(which focuses on changing actions/behaviours)

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16
Q

How does the cognitive component of CBT help treat OCD

A

Helps to stop obsessive thoughts(obsessions)

Client is encouraged to test the beliefs that the thought activates until they no longer generate anxiety

CBT helps to prevent a common cognitive distortion of catastrophising

An additional technique called habituation training is used in CBT where the client is asked to think repeatedly about their obsessive thoughts. The idea is that deliberately thinking about obsessions will cause them to become less anxiety provoking, with the consequence that compulsive is not required to reduce high levels of anxiety.

17
Q

How does the Behavioural component of CBT helps treat OCD

A

Focuses on compulsions found in OCD

the most common behavioural therapy used in CBT is known as Exposure and Response Prevention Therapy

ERPT deliberately exposes clients to objects or situations that cause anxiety and requires the client to resist performing the compulsive behaviour. The role of the therapist is to help the person develop ways in which they can resist performing the compulsive behaviours

The following steps involve:

  1. Informing the client about exposure and response prevention and what the therapy will involve
  2. Using what is called exposure hierarchy, which starts with mild anxiety raising situations and goes through to the highest level of anxiety
  3. Repeated exposure to situations that cause high anxiety, until the level of anxiety reduces
  4. Getting the client to resist and refrain from performing the compulsive behaviour
18
Q

AO3 of biological treatments

A

Side effects of BZ’s can be aggression and long-term impairment of the memory, Problems with addiction, therefore they should only be used for a limited time

From the health services perspective, drugs are cheaper

In studies using placebos vs the drug, the drug is effective(Soomro et al(2008) reviewed 17 studies of the use of SSRI’s with OD patients and found them to be more effective then placebos

Side effects of tricyclics tend to be more frequent then SSRI’s. They include hallucinations and irregular heartbeat. Therefore these are only used when SSRI’s are not effective

Effective at treating the symptoms in the short term, but little long term evidence exists(Koran et al 2007)