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Psychopathology Paper 1 > Biological approach > Flashcards

Biological approach Flashcards

1
Q

What will the biological explanation explain & treat?

A
  • OCD
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2
Q

What does the biological explanation assume about OCD?

What two explanations come within the biological explanations of OCD?

A
  • OCD is usually caused by physiological e.g. brain biochemistry, neuroanatomy (brain structural abnormalities) & genetics
  1. Genetic explanation
  2. Neural explanation
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3
Q

What had genetic evidence found about genetics in OCD?

What did Nedstadt (2000) find?

A
  • First degree relatives of people with OCD (e.g. children) have a greater vulnerability of developing the disorder
  • Nedstadt (2000) found first degree relatives of OCD sufferers had 12% chance of developing OCD vs 3% in general population
  • Genetic explanation suggests people inherit a genetic disposition to developing OCD
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4
Q

What type of gene has research found that could be responsible for OCD?
What do they do?

A
  • Candidate genes
  • Involved in regulating production of neurotransmitter serotonin, involved in OCD
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5
Q

Give an example of an impaired gene & what does it do?

Research support?

A
  • SERT gene (5-HTT)
  • If this gene is impaired it mitigates the transport of the NT (serotonin)
  • Leads to decreased levels of serotonin correlating with cases of OCD
  • Ozaki (2003): Mutation of SERT found in 2 unrelated families where 6/7 family members had OCD
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6
Q

Give an example of another candidate gene involved in cases of OCD?

A
  • Impaired COMT gene
  • COMT regulates production of NT dopamine
  • Impaired COMT leaves too much dopamine in synapse, resulting in compulsive behaviours seen in patients with OCD
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7
Q

What did Taylor (2013) find?

A
  • Identified up to 230 candidate genes potentially complicit in OCD
  • Suggests OCD is polygenetic (OCD is caused by multiple genetic variants)
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8
Q

AO3 Genetic
Research support?

A

P - Nedstadt (2010) research support
E - Reviewed twin studies finding a 0.67 (67%) concordance rate for MZ (identical) twins but 31% for DZ (fraternal) twins
E - Shows closer the genetic relationship to a sufferer the greatest risk of development of OCD
L - Suggests genetics are involved in the development of OCD

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9
Q

AO3 Genetic
Nedstadt shows other explanations?

A

P - Research shows genes cannot be the only factor in development of OCD
E - If genes were the only explanation then MZ twins would’ve shows 100% concordance rate vs 67%
E - So there must be environmental influences like imitation of social roles
L - Genetic explanation of OCD could be seen as theoretically flawed

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10
Q

AO3 Genetic
Promotes Psychology as scientific?

A

P - Strength of genetic explanation is that it promotes psychology as a science
E - Genetics can be studied objectively & reliably using DNA analysis & studying family history
E - (Concordance rates in Nedstadt)
L - Suggests genetic explanation of OCD promotes psychology as a scientific discipline

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11
Q

AO3 Genetic
Biologically reductionist

A

P - Genetic explanation is biologically reductionist as it ignores other factors that could be complicit in OCD
E - e.g. Role of early childhood trauma which has been linked to the development of OCD
E - Childhood trauma may alter neural pathways involved in emotional processing, self-regulation & habits (e.g. CSTC pathway)
L - Implies although the genetic account of OCD is scientific its an incomplete explanation of OCD

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12
Q

Outline the role of a damaged caudate nucleus & orbitofrontal cortex in the neural explanation of OCD?
(4 points)

A
  • Area of the frontal lobes in the brain are abnormal with OCD sufferers
  • Caudate nucleus (located in basal ganglia) supresses signals from Orbital Frontal Cortex OFC)
  • The then OFC sends signals to Thalamus about worrying things
  • When Caudate Nucleus is damaged it fails to supress minor ‘worry’ signals & Thalamus is alerted, which sends signals back to OFC creating a ‘worry circuit’
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13
Q

Role of low serotonin?
(2 points)

A
  • Lower levels of serotonin, influences mood regulation, anxiety, sleep & social behaviour has been linked to OCD
  • Influence of low serotonin is unclear, though one possibility is serotonin plays a role in preventing behaviour repetition which can be seen in the compulsions of OCD
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14
Q

Role of low dopamine?
(3 points)

A
  • Dopamine influences award processing in the brain & receival of awards
  • If compulsive behaviour is the ‘want’ of something to become ‘habit’ then dopaminergic release decreases prior to last time habit occurred
  • Means large volume of habit will need to be committed to gain a satisfactory dopaminergic release
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15
Q

AO3 Neural
Research support?

A

P - Research support Ursu & Carter (2009)
E - Monitored brain activity in 15 OCD patients using FMRI scans
E - They found hyperactivity in the frontal orbital cortex (FOC), exactly what the neural explanation suggests
L - Supports idea of abnormal brain structures may be a causal factor in development of OCD

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16
Q

AO3 Neural
Issues with cause & effect?

A

P - Theoretical flaw is the link between OCD & brain abnormality is merely correlational & we cannot establish cause & effect
E - Both low serotonin & impaired caudate nucleus are linked to OCD
E - However we have no before measurements so we are not sure whether NT’s/brain abnormalities have caused the OCD or have developed due to OCD
L - So, it could be these biological abnormalities are a result vs rather than a cause of OCD

17
Q

AO3 Neural
Practical applications?

A

P - Neural explanation has been practically applied to help society & 2-3% of population who suffer with OCD
E - OCD sufferers have low serotonin, we can give them medication (SSRI’s) to raise serotonin
E - This removes OCD symptoms & has been successful in helping 70% of patients
L - Shows neural explanation for OCD can reduce stress by many of those affected by OCD

18
Q

AO3 Neural
Promotes psychology as scientific?

A

P - Neural explanation can be praised for being scientific & promoting psychology as a scientific discipline
E - Neural factors in psychology can be studied objectively & in falsifiable ways
E - e.g. A damaged Caudate Nucleus can be identified using FMRI’s, likewise lower serotonin can be found by using PET scans/examining cerebrospinal fluids
L - Suggests neural explanation for OCD promotes psychology as a scientific subject, worthy of financial funding

19
Q

What strategy does the biological approach take to treat OCD?
How does this work?

A
  • Drug therapy
  • By affecting NT’s in the brain
20
Q

How are the remaining NT’s removed during synaptic transmission?
(2 ways)

A
  1. Reuptake of the remaining NT into the presynaptic neuron
  2. Breakdown of the NT in the synaptic cleft by an enzyme
21
Q

What are SSRI’s & what do they do?

A
  • Selective Serotonin Reuptake Inhibitors
  • Anti-depressant medications aiming to alleviate symptoms of OCD by increasing serotonin available in the brain
22
Q

What are two examples of an SSRI?

A
  1. Prozac
  2. Bet blockers
23
Q

How does Prozac work as an SSRI?

A
  • Prozac blocks re-uptake pump in the synapse = making more serotonin available
  • SSRI’s reduce rate of re-absorption of serotonin making more available in synaptic gap, reducing OCD symptoms
  • Due to more serotonin, some serotonin dendrites become inhibitory (prevent) reducing in number (called down-regulation)
  • Down regulation causes serotonin cells to fire rapidly increasing serotonin levels
  • Neuro-adaptation takes weeks to occur but alleviates OCD symptoms
24
Q

How do Beta Blockers work as a drug in treating OCD?

A
  • Beta blockers work on beta receptors around the body, not the brain e.g. the heart
  • These drugs block adrenaline & noradrenaline so they prevents stress reaction & bodily effects of anxiety
25
Q

AO3 drug treatment
Evidence for effectiveness of treatment?
Soomro (2009)?

A

P - Evidence for the effectiveness of drug therapy for OCD
E - OCD symptoms decline for 70% of people taking SSRI’s
E - Soomro (2009) found Pt’s in 17 studies showed significant improvement with SSRI’s vs groups receiving placebo drugs
L - So, drug treatment can effectively reduce symptoms of OCD

26
Q

AO3 drug treatment
Bad side effects may reduce effectiveness?

A

P - Unwanted side effects may reduce the effectiveness of drug therapy for OCD
E - Drug therapies can have bad side effects such as indigestion, loss of libido & blurred vision
E - Because of these side effects people may stop taking their medication
L - Implies drug therapies for OCD has an ethical dilemma, as they may not be fully protecting patients from harm

27
Q

AO3 drug treatment
Promotes psychology as scientific?

A

P - Drug therapy for OCD is very scientific
E - The drugs mode of action is objective & measurable in scientific & falsifiable ways
E - For instance, the action of antidepressants on serotonin can be studied through sophisticated PET scans/cerebrospinal fluids
L - So drug therapy for OCD is an attractive option that is not subjective

28
Q

AO3 drug treatment
Not a permanent solution?

A

P - Drugs don’t offer a permanent solution for the treatment for OCD
E - Many OCD symptoms may improve with SSRI’s, but they do not generally disappear, meaning drug treatments are only partially successful
E - When patients stop taking the drugs symptoms often return, leaving dependency on the drug to remain symptom free
L - Means drug therapy for OCD has weaknesses & perhaps other therapies e.g. CBT would be a better alternative long term

Psychopathology Paper 1 (5 decks)

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