OCD (biological) Flashcards

(19 cards)

1
Q

Behavioural chracteristics:

A

compulsions are repetitive
avoidance

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2
Q

emotional characteristics:

A

anxiety and distress,
guilt and disgust.

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3
Q

cognitive characteristics:

A

obsessive thoughts
cognitive strategies to deal with obsession
insight into excessive anxiety.

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4
Q

The biological approach: and Lewis’ study

A

If a family has it, the DNA could give a child a predisposition to it.

Lewis (1936)
37% had parents with OCD
21% had siblings with OCD

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5
Q

Candidate genes:

A
  • Names given to genes that create a vulnerability to OCD, some are responsible for developing the serotonin system.
    -5HT1-D beta gene.
  • low levels of serotonin is linked with OCD.

genetics-candidate genes
neural- seretonin.

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6
Q

OCD is polygenic:

A

OCD is caused by multiple genes, up to 230.

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7
Q

Types of OCD:

A

OCD is aetiologically heterogeneous.
so one cluster of genes in one person causes ocd in one person, but in a another it doesn’t.

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8
Q

Evaluation of genetics theory:

A

+ evidence to support (Nestadt 2010)
68% of MZ twins share OCD
31% of DZ twins share OCD
- it is difficult to differentiate between environmental and genetic factors.

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9
Q

What are the 4 biological explanations?

A

1.neural explanation
2. seratonin
3. decision-making systems
4. processing unpleasant emotions

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10
Q

1.Neural explanation: serotonin and decision making

A

Abnormal functions of transmitters in the brain.

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11
Q
  1. The role of serotonin:
A

Neurotransmitters relay info from one neuron to another through the synapse. If a person has low levels of serotonin, mood, relevant info doesn’t get transmitted, leading to a low mood.Low levels of serotonin is associated with anxiety.

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12
Q
  1. Decision making systems:
A
  1. Orbital Frontal Cortex detects worrying stimuli and decides an action.
  2. Motor Cortex does the action
  3. Basal Ganglia decides outcome if it’s good or bad. If it’s good, it send seretonin to celebrate and inhibit worrying neurons. If bad, seretonin is inhibatory, leading to inactivity (OCD).
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13
Q
  1. Processing unpleasant emotions:
A

The Parahipocampal Gyrus (part of the limbic system), functions abnormally with OCD sufferers.

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14
Q

Evalutation:

A

-Diathesis model (they may have candidate genes, they will also need an enviromental trigger.

+Role of Genes and Role of Environment = COD ( Crommer in 2007, over 50% of patients in their sample had a traumatic event causing OCD.)

-Drugs are not completely effective, it is deterministic, this could add more worry as it is a pessimistic expression.

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15
Q

Drug therapy as treatments:

A

To increase or decrease levels of neurotransmitters affecting serotonin pathways.

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16
Q

How do SSRI’s work in OCD: with drugs

A

it blocks the reuptake of serotonin so that there is more of it built up in the synapse, therefore there is more for the neurone to take up.

17
Q

Process of SSRI’s: without drugs

A

A neuron sends an electrical impulse to synapse, where it is turned chemical, axon picks up transmitters and turns it chemical, then takes it to the next synapse, etc.

18
Q

Alternative to SSRI’s:

A

If after 3-4 months it’s innefective:

  • Tricyclis, which blocks the transporter mechanicsm that reabsors seretonin and nonadrenaline, prolonging their activity. But it has more severe side effects.
  • SNRI’s increase serotonin and nonadrenaline levels. But it’s new and not much research on it.
19
Q

Evaluation:

A

+ Research support for effectiveness (Soomro in 2009) compared SSRI’s to placebo’s across 17 studies. Drugs can help some people, perhaps low serotonin is a causal factor.

+Cost effective and non disruptive.

-Serious side effects with drugs.

-Could be bias as evidence is being conducted by researchers who are sponsored by drug companies.