Psychopathology- OCD Flashcards

1
Q

What is the genetic similarity with MZ twins? and how many eggs are there?

A

share 100% of their genes and are identical twins, one egg that is split into two

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2
Q

what is the gentic similarity for DZ twins? how many eggs are there?

A

share 50% of their genes and are fraternal (non-identical) twins. 2 eggs

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3
Q

what are concordance rates?

A

indicates the percentage of twins pairs or other pairs of relatives who exhibit the same disorder

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4
Q

Migel et al (2005)- what were the concordance rates for MZ and DZ twins in terms of OCD? and what does this suggest?

A

MZ- if one identical twin has OCD there is a 53-87% chance that the other twin will also develop it
DZ- if one non-identical twin has OCD there is a 22-47% the other twin will also develop it

It suggests that OCD is more of a genetics factor rather than an environmental factor

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5
Q

Lewis 1936- what were his findings and conclusions about OCD?

A

genes are involved in vulnerability for OCD

of his OCD patients, 37% had parents with OCD and 21% had siblings with OCD. suggests it runs in families

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6
Q

Pauls et al (1995)- findings and conclusions?

A

the risk of OCD was significantly greater in first-degree relatives of OCD subjects as compared to relatives of psychiatrically normal controls

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7
Q

Diathesis stress model- what does this suggest causes OCD?

A

certain genes leave people more likely to suffer from a mental health disorder but not certain- some environmental stress is necessary to trigger the condition

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8
Q

candidate genes- what do these genes create? what system fo some of them regulate/control?

A

genes create vulnerability for OCD, some are involved in regulating the serotonin sytem

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9
Q

SERT gene- what is this responsible for?

A

the transport of serotonin across synapses, causing lower levels of serotonin which is also associated with OCD

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10
Q

COMT gene- what is this responsible for? what is one variation of this gene associated with?

A

regulating the neurotransmitter dopamine. one variation of the COMT gene results in higher levels of dompamine and this variation is more common in patients with OCD

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11
Q

GE- Nestadt et al (2010) found what?

A

review of twin studies examining OCD found 68% concordance rates for OCD in MZ twins and 31% concordance rate for DZ twins experience OCD

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12
Q

GE- Counter argue Nestadt et al by saying concordance rates are not 100%

A

environment in which people are bought up in play an important role in the development of OCD

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13
Q

GE- genes are implicated in OCD- using evidence support this statement

A

samuels et al (2007) used gene mapping and found OCD sufferers who exhibited compulsive hoarding behaviour linked to chromosome 14 behaviour- shows OCD sufferers have a genetic component to their OCD

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14
Q

GE- what does aetiologically heterogenous mean?

A

different combinations of genes are implicated in the disorder- what causes it in person A may not cause it in person B

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15
Q

GE- a genetic explanation is unlikely to provide predictive value- what does this mean?

A

cannot identify a definitive causing factor of the disorder- cant change peoples genetic makeup

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16
Q

GE- limitations of twin studies as a research method?

A

may overemphasise the role of genes when comparing concordance rates of MZ and Da twins, assume higher concordance rates in mz twins indicates a genetic component for a disorder but mz are more likely to be treated similarly than dz twins- bc identical and share same gender

17
Q

GE- reductionism -environment risk factors

A

OCD is associated with trauma, so it is clearly not entirely genetic in origin. Cromer (2007)- over half ocd patient had experienced a traumatic event in their past, was most severe in those who had suffered more than one trauma

18
Q

GE- what is the diathesis stress model?

A

the theory that mental and physical disorders develop from a genetic or biological predisposition for that illness (diathesis) combined with stressful conditions that play a precipitating or facilitating

19
Q

GE- determinism- it is biologically deterministic: predetermined what genes you inherit, therefore may inherit genes for OCD, what does this remove?

A

removes accountability- ignores environmental factors and free-will

20
Q

NE- what is serotonin?

A

a neurotransmitter- a chemical messenger in the brain

21
Q

NE- what are the 6 AO1 points for neural explanations?

A
  • low levels of serotonin link to OCD
  • SERT gene is responsible for transport of serotonin across synapse
  • high levels of activity in orbital frontal cortex (“worry circuit”), cannot switch off areas
  • ignorning impulses in turn end up as obsessions
  • COMT gene, high levels of dopamine which is also linked to OCD
  • candidate genes make people more vulnerable
22
Q

NE- research evidence for the neural explanation of OCD

A

Zohar et al (1987)- a drug reduces serotonin was given to OCD patients which enhanced their symptoms- suggests low levels of serotonin directly impacts ocd, perhaps disorder does have a biological cause

23
Q

NE-but not all sufferers respond positively to serotonin enhancing drugs, relapse is high- explain Simpson et al (2004)

A

up to 45% of patients treated with Clomipramine relapsed within 12 weeks of completing medication, which lessens the support for this neurotransmitter being the sole cause of the disorder- maybe masking symptoms rather than the cause, must be other causes

24
Q

NE- causation? relate to serotonin levels

A

unable to establish if OCD is caused by low serotonin, or if having OCD influences your serotonin levels

25
Q

NE- determinism?

A

same as genetic explanation- removes accountability, ignores environmental factors and free-will

26
Q

what are SSRI’s?

A

selective serotonin reuptake inhibitor- antidepressants that increase levels of serotonin at the synapse

27
Q

what can you to to SSRI’s to achieve optimum results

A

combine SSRI’s with CBT or other drugs

28
Q

what does tricyclic mean?

A

any class of antidepressant drugs having molecules with three fused rings

29
Q

what is GABA and what does it do?

A

GABA is a neurotransmitter that tells neurons in the brain to ‘slow down’ and ‘stop firing’ around 40% of the neurons in the brain respond to GABA

30
Q

what does SNRI stand for?

A

serotonin-norepinephrine reuptake inhibitor

31
Q

how long does drug treatments usually last?

A

12-15 weeks- dosage can be changed depending on person if not working

32
Q

The use of drug treatments for OCD in 6 AO1 points:

A

-general aim to increase or decrease level of neurotransmitter activity at synapse to reduce arousal/anxiety
- SSRIs prevent the reuptake of serotonin In pre-synaptic neuron so activity in synapse is increased
– increased stimulation of the post-synaptic neuron so normalises the worry circuit in the brain
- BZs enhance activity of GABA- quietening influence on brain
– SNRIs work on serotonin and norepinephrine given if SSRIs don’t work
– 12-15 weeks, return to doctor, may increase dosage etc

33
Q

What is a placebo drug?

A

a placebo is made to look exactly like a real drug but is made of an inactive substance

34
Q

DT- describe Soomro et al (2008) experiment

A

conducted a review of the research examining effectiveness of SSRI’s and found SSRI’s were more effective than placebos in the treatment of ocd, in 17 different trails suggesting that they are a successful treatment for OCD

35
Q

DT- cost effective?

A

compared to psychological treatments drugs are cheap and non-disruptive

36
Q

DT- side effects?

A

can have side effects; indigestion, blurred vision and loss of sex drive- worse for clomipramine

37
Q

DT- motivation?

A

Less motivation than psychological therapies- easy to administer. No commitment to attending sessions. More likely to complete the course!

38
Q

DT- root of the problem and relapse rates?

A

drugs fail to address the root cause of the OCD especially if it was a traumatic life experience - a relapse may occur when drugs are not taken as the drugs are not masking the symptoms any more