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Psychology > Psychopathology L11 - 13 (OCD) > Flashcards

Psychopathology L11 - 13 (OCD) Flashcards

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1
Q

OCD definition:

A

Anxiety disorder characterised by anxiety that arises from both obsessions and compulsions

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2
Q

Obsessions:

A

Persistent internal thoughts

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3
Q

Compulsions:

A

Repetitive external behaviours as a response to obsessions (however some may do this without obsessions)

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4
Q

Behavioural characteristics of OCD:

A
  • Compulsions –> feeling that smth dreadful will happen if they do not
  • Hinder everyday functioning
  • Avoidance –> may attempt to reduce anxiety by avoiding situations that may trigger it
  • Repetitive
  • Social impairment –> anxiety levels may prevent formation of interpersonal relationships
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5
Q

Emotional characteristics of OCD:

A
  • Anxiety + distress
  • Accompanying depression
  • Guilt + disgust –> Irrational guilt over minor issues
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6
Q

Cognitive characteristics of OCD:

A
  • Realisation of inappropriateness
  • Obsessions –> ideas, doubts, impulses + images
  • Attention bias –> hyper-vigilant w/ more attention to stimuli
  • Recognised as self-generated –> understanding that obsessions are self-thought
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7
Q

What are the two biological explanations for OCD?

A
  • Genetic
  • Neural
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8
Q

Why may OCD be inherited by sufferers and how is this usually investigated by psychologists?

A
  • May have genetic predisposition/vulnerability
  • Family/Twin studies are used
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9
Q

What has OCD been classed as, what does this mean and what are these responsible genes known as?

A
  • Polygenic –> multiple genes are responsible for the disorder
  • Candidate genes
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10
Q

How does the COMT gene cause OCD and what are its effects on the body?

A
  • Found to be more common in OCD patients
  • Regulates production of neurotransmitter dopamine
  • High levels of dopamine are responsible for drive, motivation and aggression
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11
Q

What does the SERT gene stand for, how does it cause OCD and what are its effects on the body?

A
  • Serotonin Transport gene
  • Results in low levels of serotonin
  • This means a low mood and depressive symptoms
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12
Q

What chromosome is the SERT gene on and what issue in the gene causes poorly regulated levels?

A
  • Chromosome 17
  • A mutation
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13
Q

What research support shows that it is a mutation in the SERT gene that causes OCD?

A
  • Osaki (2003) found that 6/7 family members who had OCD had this mutated gene
  • The low levels of serotonin as a result may also account for accompanying depression
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14
Q

List the strengths of the genetic explanation for OCD

A

Research support:
- Nestadt (2000) found that people who had first-degree relatives with OCD were x5 more likely to get the illness
- Billett (1998) found from a meta-analysis of 14 twin studies that OCD is 2x more likely to be concordant with monozygotic twins than dizygotic twins
- Beekman and Cath (2005)

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15
Q

What was Beekman and Cath’s study (2005) and what were the findings?

A
  • Meta- analysis of 10,034 twin studies, comparing MZ and DZ twins
  • OCD patients had been diagnosed by older criteria
  • Studies where patients had been diagnosed with DSM criteria were also examined
  • In children, OCD is transmitted genetically and genetic influence rate is from 45 - 65%
  • In adults, OCD is transmitted genetically and genetic influence rate is from 27 - 47%
  • Therefore OCD is transmitted genetically but is more apparent in children than adults
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16
Q

What are the limitations of Beekman and Cath’s research?

A
  • Maj of twin studies were not performed in controlled conditions, which questions objectivity and validity of results
  • Gene mapping (comparing DNA of twins w/ OCD and w/out) was not considered, which would be needed to make results more valid
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17
Q

List the weaknesses of the genetic explanation

A
  • Concordance rate for OCD is not 100%, therefore it is not entirely caused by genetics. Other factors eg environmental/psychological may be involved
  • Polygenic so it could be that it is only a predisposing factor rather than one responsible gene.
  • Cause is very complex as it is also genetically linked to other illnesses eg Tourette’s + Autism
  • Behavioural approach contradicts cognitive approach, as all behaviour can be learnt (classical + operant conditioning). The foremost has a lot of support and OCD is often treated w/ behavioural therapies
  • Diathesis stress model argues the opposite, that OCD can be caused by genes but also a trigger in the environment
18
Q

How do high levels of dopamine and low levels of serotonin affect parts of the brain (which parts?) respectively?

A
  • Over activity in basal ganglia area in frontal lobes
  • Malfunctioning in caudate nucleus in frontal lobes
19
Q

Where in the brain is the basal ganglia, what is this responsible for and how does its malfunction lead to symptoms of OCD?

A
  • Orbital frontal cortex
  • Responsible for motor functions, habit learning, cognition + emotion
  • Malfunction results in repetitive motor functions
20
Q

What are the strengths of the neural explanation for OCD?

A
  • Research support
21
Q

What are the weaknesses of the neural explanation?

A
  • Cause and effect is unclear –> high levels of dopamine and low levels of serotonin may actually be an effect of OCD, not the cause
  • Unclear whether low levels of serotonin cause OCD, depression or both as they are co-morbid
  • Not enough research evidence to show high levels of dopamine directly cause OCD –> they also cause bipolar depression and schizophrenia
22
Q

What research support on animals shows that enhanced dopamine levels can induce OCD?

A

High does of drugs used on animals showed that dopamine levels were enhanced, which induced movements that resembled compulsive and repetitive behaviour. This is similar to OCD sufferers.

23
Q

What research was conducted in 2000 that showed high levels of dopamine were possibly a cause for OCD?

A
  • Ciccerone (2000) found low doses of drug Risperidone helped lower levels of dopamine and alleviate some symptoms
  • Therefore high levels of dopamine may be a cause for OCD
24
Q

What research was conducted in 2007 that showed an abnormality in brain structure in OCD sufferers?

A
  • Menzies (2007) studied MRI scans in OCD patients and their immediate family and compared them to healthy controls
  • OCD patients and their family had an unusual neuroanatomy and reduced grey matter in key regions of the brain
  • Abnormal brain structure, causing abnormal levels of neurotransmitters, could be inherited via genes therefore supporting the neural explanation
25
Q

What is the neuroanatomy explanation for OCD?

A
  • OCD may be caused by some types of brain damage, which might have been caused by a virus
  • Damage may cause problem in short-term memory which causes a chain reaction of doubts that result in repetitive behaviour
26
Q

Who explored the neuroanatomy explanation and what did they do?

A
  • Jenike and Rauch
  • OCD patients studied using PET (position emission tomography) scans. When shown an image of smth dirty, the frontal lobes and basal ganglia (possibly overactive) were the most active parts of the brain.
27
Q

What research supports the neuroanatomy/neural explanation?

A
  • Rapoport (1990) reviewed an epidemic that occurred in Europe between 1916-1918 called the Great Sleeping Sickness (widespread viral brain infections)
  • After epidemic, major rise in number of reported OCD cases, which may have been due to damage caused by the viral infection
28
Q

What are two drug treatments used to treat OCD and give examples for one

A
  • SSRI (Selective Serotonin Re-uptake Inhibitors eg. Prozac + Fluoxetine
  • SNRI (Selective Norepinephrine Reuptake Inhibitors) –> new type of drug
29
Q

How do low serotonin levels usually affect anxiety?

A
  • Implicated in ‘worry circuit’
  • This is where damage to caudate nucleus in brain fails to suppress minor worry signals
  • Message sent to orbital frontal cortex
  • Anxiety worsens
30
Q

What do SSRI drugs prevent and how does it do this?

A
  • Prevent reuptake of serotonin
  • By prolonging its activity in the synapse
31
Q

What is the effect of increased serotonin levels?

A
  • Implication of worry circuit reduced
  • Helps orbital frontal cortex to function normally
  • Stabilise mood
  • Improve memory (reducing compulsive behaviour)
32
Q

What is a synapse?

A

Gap between 2 nerve cells where impulses pass by the diffusion of a neurotransmitter

33
Q

How long are SSRI drugs prescribed for?

A

12 -16 weeks

34
Q

What two neurotransmitters does SNRI increase and who is this drug most suitable for?

A
  • Increases serotonin + noradrenaline/norepinephrine
  • Suitable for patients who cannot tolerate SSRI
35
Q

What is norepinephrine and what does it aim to do?

A
  • Neurotransmitter released from sympathetic nervous system in response to stress
  • Mobilise brain and body for action
36
Q

List the strengths of SSRI drugs:

A
  • Research support –> Soomro (2009) reviewed 17 studies, comparing SSRI’s performance to placebo drugs, where all of them showed SSRI was more effective, especially when combined w/ CBT
  • Relatively effective –> 70% of patients experienced decline in symptoms after usage
  • Cost-effective in comparison to psychological therapies like CBT, counselling –> good value for NHS
37
Q

List the weaknesses of SSRI drugs:

A
  • Only most effective if combined w/ other treatments –> 30% tended to opt for psychological therapies/ combo of SSRI + this
  • Do not work for all OCD patients –> may need alternative eg. tricyclics (diff drug)
  • Terrible temporary side effects eg. indigestion, blurred vision, loss of sex drive
  • Koran (2009) said psychotherapies should be used first, even though drug therapy is more popular and a quick fix, as SSRI does not provide lasting cure for OCD + many patients relapse a few weeks after stopping drugs
38
Q

What other drugs are there that control the action of neurotransmitters and give two examples

A

BZ (Benzodiazepine) drugs eg. Valium + Xanax

39
Q

What does BZ reduce and give one limitation of one of these?

A
  • BP
  • Heart rate
  • Activity in CNS
  • Brain arousal
  • Serotonin levels –> Lower arousal so anxiety is reduced, however more likely to get depressed
40
Q

How do BZ drugs work?

A
  • Increases GABA (Gamma-Amino butyric acid) –> neurotransmitter that slows down firing of neurons
  • BZ drug binds to GABA receptor site of post synaptic neuron
  • Chloride ion flow increased (makes it more difficult for neuron to be stimulated by other neurotransmitters)
  • Neuron activity slowed down, making person less anxious
41
Q

List the strengths of BZ drugs:

A
  • Very effective –> Used on global basis
  • Quicker + more effective than other psychological treatments eg. CBT –> relief can be seen immediately
  • Can be used for short periods of time w/ barely any serious side effects
42
Q

List the weaknesses of BZ drugs:

A
  • Several unwanted side effects if used long term –> eg. drowsiness, depression, unpredictable interactions w/ alcohol
  • Ashton (1977) found long-term users become very dependent + sudden withdrawal leads to high level of anxiety. Issue of drug escalation, where high doses of drug needs to be taken to reduce symptoms if being used long term
  • Causes temporary cognitive impairment –> Stewart (2005) carried out meta analysis and found out long-term use causes this. Ability improves after drugs are withdrawn but never fully return to the level before drugs

Psychology (30 decks)

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