Psychopathology Flashcards

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1
Q

statistical infrequency

A

statistical infrequency: defining what is most common or normal using typical values, so we also have an idea of what is not common. example is high IQ.

AO3:
some abnormal behaviours are desirable such as high IQ.
using s.i. means we are unable to distinguish between desirable and undesirable behaviours.

cut-off point is subjective when deciding where to separate normal from abnormal. some may think abnormal sleep is 6 hours and some may think it is 5.

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2
Q

deviation from social norms

A

deviation from social norms: norms created by a group of what is socially acceptable behaviour. anyone who behaves differently is considered abnormal. homosexuality was based on social deviation and considered a mental illness.

AO3:
distinguishes between desirable and undesirable. provides a way to notice undesirable and damaging behaviours so that the person can receive help.

context needs to be considered. wearing almost nothing on a beach is considered normal but in a school it would be abnormal or even a mental disorder. social deviance on its own is not a complete explananation.

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3
Q

failure to function adequately

A

not being able to cope with everyday living and causing distress to themselves or others.
eating regularly, washing clothes, going to work, communicating.
using DSM abnormality is given a quantitative measure out of 180.

AO3:
it is subjective - the ‘abnormal’ person may be content with their situation or unaware, it is only others that judge them as abnormal. judgement depends on who is making the decision.

failure to distinguish between functional and dysfunctional behaviours - depression may lead to paying more attention - it is rewarding and functional.

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4
Q

deviation from ideal mental health (Marie Jahoda)

A
the absence of the following criteria shows abnormality and mental disorder.
self-attitudes (high self esteem)
self-actualisation (personal growth)
integration (dealing with stress)
autonomy (independent)
accurate perception of reality
mastery of the environment 

AO3:
unrealistic as most people lack something and how many need to be lacking to be considered abnormal.
it is difficult to measure capacity for personal growth.
not usable.

self-actualisation is relevant to individualistic cultures but not collectivist, where they put the needs of the group above their own.
usefulness is limited to certain cultures.

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5
Q

the behavioural approach to explaining phobias

A

two process model:

classical conditioning initiates the phobia.
Little Albert:
UCS = loud noise, UCR = fear and NS = furry object
pairing loud noise with furry object lead to fear response (CR). the furry object is now a CS.

operant conditioning maintains the phobia.
the avoidance of the phobic stimulus reduces fear and is reinforcing. this is negative reinforcement.

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6
Q

how else can phobias be aquired

A

through modelling (social learning)

children seeing a parent respond to spider with fear, and gaining attention which seems awarding.
so the child acquires this behaviour.

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7
Q

behavioural approach to phobias AO3

A

two process model is supported by research into peoples phobias. people often recall a specific incident leading to their phobia and even if they dont it is likely they have forgotten the traumatic experience.

biological preparedness: humans are genetically programmed to make associations between life threatening stimuli and fear. in our evolutionary past, snakes and heights may have been life threatening, leading to fear. we are less likely to develop a fear of modern objects. behavioural approach cannot explain all phobias.

it ignores cognitive factors such as fears being caused by irrational beliefs.

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8
Q

systematic desensitisation

A

counterconditioning: patient is taught new association through classical conditioning, such as relaxation.

relaxation is the first thing that the patient is taught, such as slow and deep breaths.

desensitisation hierarchy:
gradually introducing feared stimuli from least to most feared so that patient isn’t overwhelmed.
1. taught relaxation
2. desensitisation hierarchy created
3. gradually works through each stage using relaxation
4. masters feared stimulus

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9
Q

SD AO3

A

success: 75% patients respond well. in vivo techniques are most effective, so range of techniques is important.

is only effective for some phobias, those acquired through experience. not appropriate to treat evolutionary phobias such as fear of the dark.

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10
Q

flooding

A

patient immersed in experience for one long session, continuing until anxiety has disappeared.

a person’s fear response always has a time limit.
as adrenaline naturally decreases, the feared stimulus is associated with non-anxious response.

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11
Q

flooding AO3

A

flooding is quicker than CBT and is reported as more effective than SD.

it is not for every patient as it can be highly traumatic. patients may quit mid treatment, reducing its effectiveness.

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12
Q

behavioural therapy AO3

A

they lack the need for thinking, unlike CBT, so is suitable for patients such as children or those with learning disabilities.

only treating symptoms causes symptom substitution, it is more important to treat the underlying cause. Little Hans developed a phobia of horses but his actual problem was envy of his father. once the feelings about his father were resolved, the phobia was cured.

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13
Q

biological approach to explaining OCD - COMT gene

A

COMT gene - COMT regulates production of dopamine. one form of this gene is more common in OCD patients than people without the disorder. It produces lower activity of COMT gene and higher dopamine levels.

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14
Q

SERT gene - genetic

A

SERT gene - affects transport of serotonin, creating lower levels of this neurotransmitter. Study of two unrelated families which had this mutated gene and 6/7 members had OCD.

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15
Q

Diathesis-stress - genetic

A

genes such as SERT are implicated in other disorders such as depression.

each gene creates a vulnerability (diathesis) for mental conditions.
stressors affect what condition develops.

could have COMT or SERT gene but have no illness.

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16
Q

abnormal levels of neurotransmitters - neural

A

dopamine levels abnormally high in OCD.

animal study - drugs increasing dopamine induced stereotyped movements of compulsions in OCD patients.

antidepressants that increase serotonin levels, reduce OCD.
antidepressants with less effect on serotonin do not reduce OCD.

17
Q

abnormal brain circuits - neural

A

when caudate nucleus is damaged it fails to suppress minor worry signals
thalamus is alerted
sends signals to orbitofrontal cortex, acting as a worry circuit

supported by PET scans taken whilst symptoms are active, showing OFC activity.

abnormal levels of serotonin can cause OFC and caudate nuclei to malfunction.
high dopamine levels lead to overactivity in basal ganglia (caudate nucleus).

18
Q

OCD AO3

A

neurotransmitter study on animals - application to humans is too simple

competition of psychological explanations - two process model for OCD.
NS (dirt) associated with anxiety. maintained as anxiety provoking stimulus is avoided. obsession formed when compulsive behaviour appears to reduce anxiety.

support - MRI produce images of OCD patients, immediate family and unrelated healthy people. patients and relatives had reduced grey matter in OFC - so inherited and may lead to OCD.

genes not unique to OCD but are a predisposing factor to obsessive behaviour. the same gene is found in tourettes, autism. obsessive behaviour is anorexia.

19
Q

OCD drug therapy - SSRIs

A

low levels of serotonin are involved in the worry circuit, so increasing serotonin may normalise this circuit.

antidepressants reduce anxiety linked to OCD.

serotonin regulates anxiety and SSRIs inhibit the reuptake of serotonin at the presynaptic membrane.

20
Q

OCD drug therapy - tricyclics

A

they block transporter mechanism that reabsorbs serotonin and noradrenaline into presynaptic cell after it has fired.

more neurotransmitters are left in synapse, prolonging activity.

they can target more than one neurotransmitter.

have strong side effects so used as second option.

21
Q

OCD drug therapy - anti-anxiety drugs

A

they slow down activity of CNS by enhancing activity of neurotransmitter GABA, which has a quieting effect on neurons in brain.

it reacts with GABA receptors on outside of receiving neurons.
this opens a channel to increase flow of chloride ions into neuron, which makes it harder for neuron to be stimulated by other neurotransmitters, slowing activity and causing relaxation.

22
Q

treating OCD - AO3

A

not a lasting cure - patients relapse within a few weeks of stopping meds.
recommended that psychotherapies, CBT, are used first.
exposure and response prevention, similar to systematic desensitisation.

side effects - nausea, headache and insomnia are common from SSRIs. this is often enough for patient to stop drug.
anti-anxiety drugs have risk of addiction so usage is limited to 4 weeks.

effectiveness - 17 studies of SSRIs reviewed and they were more effective than placebos in reducing OCD symptoms.
however, most of these studies only have a 3 month duration - long term effectiveness not known.