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psychopathology > OCD > Flashcards

OCD Flashcards

1
Q

OCD

A

anxiety disorder
- characterised by the DSM-V
- repetitive behaviour (compulsions) and obsessive thinking

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2
Q

behavioural characteristics of OCD (5)

A

COMPULSIVE BEHAVIOUR
HINDER EVERYDAY FUNCTIONING
- obsessive/forbidden ideas creates lots of anxiety
- could lead to compulsions & repetitive behaviour
- seriously hunger ability to perform everyday functions, like having a job
SOCIAL IMPAIRMENT
- anxiety levels and compulsive behaviour might become so high they cannot conduct meaningful interpersonal relationships
REPETITIVE
- repeat behaviours over and over again
- response to obsessive thoughts, ideas, images
AVOIDANCE
- some reduce anxiety by avoiding situations that might trigger it
- can lead to further problems

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3
Q

compulsive behaviours: behavioural characteristic of OCD

A

performed to reduce anxiety created by obsessions
- repetitive & unconcealed
- eg hand washing or checking things
- could include mental acts, like praying/counting
- feel they must do these things otherwise smthn dreadful might happen
- external components - can be seen by others

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4
Q

emotional characteristics of OCD (3)

A

ANXIETY & DISTRESS
- obsessions + compulsions = source
- aware that compulsive behaviours are excessive
— causes embarrassment and shame
- cannot consciously control their compulsive behaviour
— distress
ACCOMPANYING DEPRESSION
- low mood
GUILT & DISGUST
- irrational guilt over minor issues
- disgust directed either externally (eg dirt) or internally

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5
Q

cognitive characteristics of OCD (4)

A

OBSESSIONS
RECOGNISED AS SELF GENERATED
- understand obsessive thoughts, impulses, images are self invented
REALISATION OF INAPPROPRIATENESS
- cannot consciously control or stop thoughts
- know they’re inappropriate / irrational
ATTENTION BIAS
- perception tends to be focused on anxiety generating stimuli
- eg focussing on dust on the table that has just been cleaned
- tend to be hyper vigilant & look for things to justify their anxiety

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6
Q

obsessions: cognitive characteristic of OCD

A

recurrent, intrusive thoughts/impulses
- perceived as inappropriate or forbidden
- may be frightening or embarrassing
- common themes include ideas, doubts (cooker is off?), impulses (shout/swear in public), or images (sexual)
- uncontrollable and cause anxiety
- internal - occur in the mind

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7
Q

biological approach to explaining OCD

A

assumes OCD is caused by genetics and neural explanations

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8
Q

genetic causes of OCD

A

COMT and SERT gene
- may be inherited whereby sufferers have a genetic vuln. or predisposition to get the illness
- polygenic = one single gene is NOT responsible, many genes = responsible (candidate genes)

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9
Q

COMT gene

A

regulates production of dopamine (neurotransmitter)
- HIGH levels of dopamine associated w OCD
- dopamine responsible for drive, motivation, aggression
- gene found to be more common in OCD patients

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10
Q

SERT gene

A

effects transportation of serotonin
- results in LOW levels of serotonin
- low mood and depressive symptoms
- this gene on chromosome 17, it seems a mutation in this gene can cause OCD
- Ozaki (2003) found that 6/7 family members who had OCD has a mutation of the SERT gene
- link w OCD and depression

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11
Q

strength of genetic explanations - OCD

A

Nestadt (2000) supports the genetic explanation for OCD
- found that ppl who had a FIRST DEGREE RELATIVE who alr had OCD were 5X MORE LIKELY to also get the illness
- supports the idea that OCD is transmitted genetically

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12
Q

strength of genetic explanations for OCD

A

Billett (1998) supports the idea that it’s transmitted genetically
- did a META-ANALYSIS of 14 twin studies
- found OCD is 2X more likely to be concordat in IDENTICAL monozygotic twins (rather than dizygotic identical twins)
- supports the idea that it’s transmitted by genetics

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13
Q

criticism of genetic explanation

A

the CONCORDANCE RATE for OCD is NOT 100%
- so, it cannot be caused entirely by genetic factors
- explanation fails to take into account PSYCHOLOGICAL & environmental factors (that might contribute to cause of OCD)

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14
Q

criticism of genetic explanation

A

it’s POLYGENIC
- one single gene is not responsible for causing it
- it’s been genetically linked to other illnesses, eg tourette’s syndrome & autism
- therefore, it seems that genetic cause is very COMPLEX
- and might be related to other illnesses too
- could be that one specific gene is not responsible for it, but it could be a predisposing factor

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15
Q

weakness of genetic explanation (behavioural approach)

A

behavioural approach would CONTRADICT the genetic explanation
- two process model would suggest that OCD can be LEARNT via classical conditioning
— rewarded through reinforcement (operant conditioning)
- behavioural approach gained a great deal of support in explaining cause of OCD
- often treated using behavioural therapies (eg exposure, similar to SD)

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16
Q

weakness of genetic explanation

A

the diathesis model would argue OCD can be caused by a combination of genes AND a trigger in the environment (stress)
- therefore, genes alone cannot be the only cause of it
- genes would need to be COMBINED w other factors in order for the disorder to develop
- the diathesis stress model would WEAKEN the genetic argument

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17
Q

Beekman and Cath twin studies

A

META ANALYSIS
- MZ twins compared w DZ twins
- 10034 twin pairs studied overall
- results in CHILDREN : ocd is inherited via GENES
— (genetic influence ranges from 45%-65%)
- results in ADULTS : ocd is inherited via GENES
— (genetic influence is 27%-47%)
- conclusion = ocd transmitted genetically, this is more apparent in children)

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18
Q

weakness of Beekman and Cath’s research

A

majority of the twin studies were NOT performed in CONTROLLED CONDITIONS
- means that the data is NOT very OBJECTIVE, or scientific
- might affect the validity and reliability of the results gained
- might question the idea that ocd is genetic

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19
Q

criticism of Beekman and Cath’s research

A

GENE MAPPING was NOT taken into consideration
- when looking at whether ocd = genetic
- gene mapping would look closely at the DNA of the twins that had ocd
— compare w twins that don’t have ocd
- COMPARISON needs to be made in order to make the results more valid

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20
Q

strength of Beekman and Cath’s research

A

META ANALYSIS = strong
- multiple diff. studied and combining them
- results = more accurate

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21
Q

neural explanations of OCD

A

neurotransmitters : dopamine and serotonin

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22
Q

dopamine (neural explanation)

A
  • neurotransmitter that affects mood, might be a cause
  • FRONTAL LOBES in the brain have been linked to dopamine activity
  • ocd - high levels
  • high levels have also been linked to over activity in the BASAL GANGLIA (in the brain)
  • research found that high does of dopamine enhancing drugs can induce movements that resemble compulsive and repetitive behaviour, similar to OCD symptoms
23
Q

serotonin (neural explanation)

A
  • FRONTAL LOBES in the brain have been linked to serotonin activity
  • ocd = low levels, can cause depressive like symptoms + obsessive thoughts
  • serotonin plays key role in operating the CAUDATE NUCLEUS in the brain
    — low levels cause it to malfunction
24
Q

strength of neural explanations

A

great deal of RESEARCH SUPPORT
- state that neurotransmitters do cause OCD
- anti-depressant drugs will inc. serotonin levels in ocd patients
— had led to a reduction of ocd symptoms
- therefore, there is good evidence to suggest that low levels of serotonin could be a cause of ocd

25
Q

disadvantage of neural explanations

A

CAUSE and EFFECT
- neurotransmitters might not necessarily CAUSE ocd
- instead, low serotonin + high dopamine might be the EFFECT of ocd
- so, we must be cautious when looking at cause & effect of neurotransmitters

26
Q

disadvantage of neural explanations

A

ocd is co morbid w DEPRESSION (exists alongside it)
- therefore, it’s NOT CLEAR whether low levels of serotonin cause ocd, depression or both
- so, the link between low levels of serotonin causing ocd is not very clear and needs to be INVESTIGATED FURTHER

27
Q

strength of neural explanations

A

research conducted by Ciccerone (2000)
- found that giving ocd patients low does of the drug Risperidone helped to LOWER DOPAMINE levels
— and alleviate some of the ocd symptoms
- so, high levels of dopamine could be a biological cause for ocd

28
Q

strength of neural explanations

A

Menzies (2007) suggested research evidence
- that would support a genetic link to abnormal levels of neurotransmitters
- studied MRI scans in ocd patients AND their immediate family members
— compared them w healthy controls
- found that ocd patients & their families had REDUCED grey matters in key regions of the brain
— &they had an UNUSUAL neuroanatomy
- concluded that ocd CAN be caused by ABNORMAL brain structure
— which could be inherited via genes

29
Q

weakness of neural explanations

A

role of DOPAMINE causing ocd has been QUESTIONED
- it’s been found that high levels of dopamine can also cause OTHER psychological illnesses (not just ocd)
— eg bipolar depression + schizophrenia
- so, not enough research evidence to suggest high dopamine can cause ocd to occur
- a COMBINATION of factors might be responsible

30
Q

Jenike and Rauch - research : neural explanations ocd

A

might be a relationship between ocd being caused by some types of brain damage which might be caused by a virus
- brain damage may cause a problem in STM that causes a chain reaction
— person doubting whether they have performed certain actions
- might then result in repetitive behaviour

31
Q

how were OCD patients studies - Jenike and Rauch

A

PET scans
- patients w cleaning obsession were shown something dirty
- evidence found that the frontal lobes and basal ganglia were the most active parts of the brain
— basal ganglia might be overactive & seems to malfunction in ocd sufferers

32
Q

what is the basal ganglia?

A

series of interconnected brain structures at the front of the brain
- near the orbital frontal cortex
— which also seems to be overactive in ocd patients
- BG is responsible for control of voluntary motor movements, procedural learning, habit learning, eye movements, cognition, and emotion
— overactive BG can lead to repetitive motor functions

33
Q

anti depressants : SSRI drugs

A
  • selective serotonin reuptake inhibitors
  • eg Prozac and Fluoxetine
  • drug aims to PREVENT REUPTAKE of serotonin and PROLONG its ACTIVITY in the synapse
  • person will feel less anxious and have HIGHER serotonin levels
  • prescribed for 12-16 weeks
34
Q

low levels of serotonin are also implicated in the …

A

‘worry circuit’, whereby damage to the CAUDATE NUCLEUS in the brain fails to suppress minor worry signals
— message then sent to orbital frontal cortex, worrying gets worse

35
Q

why does increasing serotonin levels help OCD patients?

A

helps regulate mood & reduce anxiety levels
- inc. serotonin via SSRI drugs will also help to normalise and reduce the ‘worry circuit’
- high serotonin helps the orbital frontal cortex to function at normal levels
- helps stabilise moods and emotions and improve memory
— so, it will reduce compulsive behaviour and checking

36
Q

SNRI drugs (not on spec i don’t think)

A

selective norepinephrine reuptake inhibitors
- new type of drug
- inc. serotonin and noradrenaline / norepinephrine
- suitable for ocd patients that can’t tolerate ssri drugs

37
Q

strength of SSRIs

A

SUPPORTING EVIDENCE that they’re an effective treatment
- soomro (2009) reviewed 17 studies that compared SSRIs to placebo drugs
- found that all studies showed SSRIs were more effective than placebos
- especially when combines w CBT

38
Q

evaluation of SSRI drugs (%)

A

RELATIVELY EFFECTIVE
- 70% of patients have experienced a DECLINE in ocd SYMPTOMS when taking them
- however, remaining 30% tend to opt or psychological therapies
— or a combination of SSRIS and therapy
- might mean that the drugs are most effective if COMBINED w other treatments

39
Q

benefit of SSRIs

A

relatively CHEAP and COST EFFECTIVE
- in comparison to psychological therapies (cbt)
- good value for money for the NHS, and is economical (compared to other treatments)

40
Q

criticism of SSRIs

A

they DON’T WORK for ALL patients
- for some patients, the drug will not alleviate their ocd symptoms
- they’ll have to take another drug instead which might be more effective (eg tricyclics)

41
Q

problem w SSRIs

A

terrible SIDE EFFECTS
- might mean that the patient stops taking them
- effects are temporary
- include indigestion, blurred vision, loss of sex drive

42
Q

criticism of drugs for treating OCD

A

Koran (2007) stated that drug therapy might be common/popular BUT PSYCHOTHERAPIES should be tried FIRST
- eg CBT
- drug therapy requires little effort
— might be effective short term
- but it doesn’t provide a LASTING CURE
- many patients relapse within a few weeks if the medication is stopped

43
Q

BZ drugs

A
  • Benzodiazepines
  • eg valium and xanax
  • help reduce anxiety
  • aim to control the action of neurotransmitters
  • reduce activity in the CNS and reduce brain arousal
  • reduce blood pressure and reduce heart rate
44
Q

GABA

A

GABA = neurotransmitter in the brain
- slows down the firing of neurons
- makes the person less anxious & calmer
- helps reduce psychological activity in the body

45
Q

GABA & BZs

A
  • BZ drugs BIND to the GABA RECEPTOR SITE of the post synaptic neuron
  • this increases the flow of CHLORIDE IONS into the POST SYNAPTIC NEURON
    — makes it more difficult for the neuron to be stimulated by other neurotransmitters
    — thus SLOWING down its activity & making the person feel more RELAXED
  • neurons in the brain become LESS ACTIVE - feels calmer
46
Q

what is a post synaptic neuron?

A

neuron that receives the signal (from a synapse)

47
Q

however, BZs decrease …

A

SEROTONIN
- means that the person has lower arousal and reduces anxiety
- BUT = less happy
- more likely to get depressed

48
Q

strength of BZs

A

very EFFECTIVE at reducing anxiety & ocd symptoms
- used by millions of people worldwide
- so they’re very good at reducing anxiety & ocd on a GLOBAL BASIS

49
Q

advantage of BZs

A

work very QUICKLY & effectively to cure ocd symptoms
- compared to other psychological treatments
- BZs can begin to reduce anxiety levels and ocd symptoms in a short period of time
- person will see some IMMEDIATE BENEFITS f relief

50
Q

strength of BZs

A

can be used for a SHORT PERIOD of time with HARDLY ANY serious SIDE EFFECTS
- unlike other types of drugs
- so, side effects are kept to a minimum in the short ter,
- good for the patient

51
Q

problem w BZs

A

if they are used LONG TERM, then several unwanted SIDE EFFECTS can begin to appear
- eg drowsiness, depression, unpredictable interactions w alcohol
- patients have high chance of being involved in accidents
- so, BZs should NOT be used as a long term treatment

52
Q

weakness of BZs

A

Ashton (1997) found that long term users become very DEPENDANT on the drug
- sudden withdrawal can lead to a return of high anxiety & ocd symptoms
- problem of DRUG ESCALATION
— whereby patients need to take very large doses of the drug in order to reduce ocd symptoms (if they take the drug for a long period)

53
Q

criticism of BZs

A

Stewart (2005) criticised LONG TERM use of BZs
- bcs they cause IMPAIRMENT in speed & processing of VERBAL LEARNING
- effects = temporary (but are still -ve)
- carried out a meta analysis
— found clear evidence that long term use leads to COGNITIVE IMPAIRMENTS
- (cognitive ability seems to improve one BZs are withdrawn, but it’s still below that of control patients who have never taken them)

psychopathology (4 decks)

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