OCD Flashcards

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1
Q

What are the behavioural characteristics of OCD

theres 2

A
  • Compulsions - repetitive actions to reduce anxiety stemming from obsessions
  • Avoidance - attempt to reduce anxiety by avoiding situations that may trigger it
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2
Q

What are the emotional characteristics of OCD

theres 2

A
  • Anxiety - stems from awareness of behaviour being excessive and know they can’t control themselves, feeling shame
  • Disgust - either at self or at external sources
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3
Q

What are the cognitive characteristics of OCD

theres 3

A
  • Obsessions - recurrent intrusive irrational thoughts which cause anxiety
  • Awareness of Irrationality - sufferers understand their behaviour and thoughts are inappropriate but they still can’t control it
  • Catastrophic Thinking - worried that if they do not carry out compulsion, something bad will happen (irrational)
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4
Q

What’re the two biological explanations of OCD & the assumptions

assumptions of the biological explanations

A
  • Genetic explanation
  • Neural explanation
  • caused by genetic and biochemical factors
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5
Q

What is the genetic explanation of OCD

A
  • OCD is classed as polygenic (many candidate genes responsible for causing)
  • COMT gene - regulates dopamine production. High dopamine associated w/ OCD.
  • Variation of COMT gene that produces higher levels of dopamine is common with OCD patients
  • SERT gene - affects transportation of serotonin. Causing lower levels. Low serotonin is linked to OCD
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6
Q

What is the neural explanation of OCD

A
  • abnormal levels of neurotransmitters are associated with OCD (dopamine+serotonin)
  • high dopamine levels are linked to hyperactivity in the basal ganglia area in the brain (causes compulsions)
  • low levels of serotonin in the caudate nucleus in the basal ganglia cause the caudate nucleus to malfunction (causes obsessions)
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7
Q

Research Support for genetic explanation

(+) smth about relatives n OCD idk

Nestadt(2000)

A

found that people with a first degree relative with OCD were five times more likely to have OCD

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8
Q

Research Support for genetic explanation

(+) Meta-analysis of 14 twin studies

Billett(1998)

A

OCD is 2x more likely to be concordant in identical monozygotic twins rather than dizygotic (non identical)

found from a meta-analysis of 14 twin studies

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9
Q

(-) smth about concordance rates

weakness for genetic explanation

A
  • Concordance rate in identical twins is not 100%

Thus fails to account psychological and environmental factors

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10
Q

(-) Biological approach contradicts with behavioural approach.

A

Two process model suggests that OCD is learnt via classical conditioning and reinforced through operant conditioning

OCD is often treated with behavioural therapies such as exposure (similar to SD)

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11
Q

Strength for neural explanation

(+) Antidepressants work

A

Antidepressants increase serotonin levels

Has shown reduction in OCD symptoms

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12
Q

Strength for neural explanation

(+) Risperidone

Ciccerone(2000)

A

found giving patients low doses of drug Risperidone to lower dopamine caused symptoms of OCD to alleviate

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13
Q

Weakness of neural explanation

(-) Cause n effect

A

Neurotransmitters may not necessarily cause OCD but rather just a symptom

(low serotonin, high dopamine)

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14
Q

Weakness for neural explanation

(-) Co-morbidity

A

OCD is co morbid with depression

It is unclear if low serotonin causes OCD or depression or both

Link is unclear

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15
Q

What is the biological treatment for OCD

A
  • Uses medication to increase/decrease neurotransmitter levels

-general purpose to decrease heart rate, anxiety, low arousal, blood pressure

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16
Q

What are selective serotonin re-uptake inhibitors (SSRIs)

A
  • Serotonin release by presynaptic neurons.
    -Travel across synaptic cleft.
  • Chemically convey signal from presynpatic neuron to postsynaptic neuron
    -reabsorbed (re-uptake) by presynaptic neuron
    -broken down and reused

SSRIs prevent reabsorption & breakdown of serotonin.
-increase levels in synapse
-continues to stimulate postsynaptic neuron
-reduces anxiety

17
Q

What are benzodiazepines (BZs)

A
  • Anti-anxiety drugs (Valium, diazepam)

Slow activity of CNS by enhancing neurotransmitter GABA (has inhibitory effects on neurons)

  • GABA reacts with GABA receptors outside neurons
    -GABA locks into these receptors
    -opens channel to increase chloride ion flow into neuron

Chloride ions make it harder for neuron to be stimulated by other neurotransmitters (slows down neural activity, makes person relaxed)

18
Q

(+) Research support for SSRIs

Soomro(2009)

A

reviewed 17 studies comparing SSRIs with placebos

-all 17 studies showed SSRIs were more effective especially when combined with CBT

19
Q

(+) SSRIs work

A

70% of patients that take SSRIs see a decline in symptoms

30% opt for psychological therapies or a combo of both

20
Q

SSRIs weakness

(-) Side effects

A

Severe side effects meaning they may stop taking it making it ineffective

-Symptoms include indigestion, blurred vision, loss of sex drive

21
Q

(+) Benzodiazepines work

A

reduce anxiety levels and OCD symptoms quickly, compared to CBT where patient doesn’t experience immediate relief

22
Q

(-) Side effects of benzodiazepines

A

if used long-term then side effects appear
-side effects include drowsiness, depression, unpredictable interactions with alcohol

23
Q

(-) Becoming dependent on benzodiazepines

Ashton(1997)

A

found long-term users to become dependent and experience high levels of anxiety + symptoms with withdrawal.

-patients need progressively larger doses to reduce symptoms because tolerance (body gets used to drug)