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AQA Psychology (A Level) > Psychopathology > Flashcards

Psychopathology Flashcards

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1
Q

(DoAbnormalities) What is Failure to function adequately?

A

When you can’t function enough to meet normal human requirements such as working or eating and this causes observer discomfort.

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2
Q

(DoAbnormalities) What is an advantage of the FFA definition?

A

There is psychological realism to this definition, as we can see a lack of motivation to do daily activities such as working/eating in depressed individuals.

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3
Q

(DoAbnormalities) What is a disadvantage of FFA?

A

It lacks cultural relativism - can we really generalise activities we class as necessary, necessary for all types of cultures?

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4
Q

(DoAbnormalities) What is DSN?

A

Deviation from Social Norms: when the individual is behaving in an antisocial manner which goes against what is deemed socially acceptable e.g. drunk driving.

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5
Q

(DoAbnormalities) What is an advantage of DSN?

A

Again, has psychological realism; behaviours which aren’t classed as ideal by the majority tend to be signs of abnormalities.

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6
Q

(DoAbnormalities) What are disadvantages of DSN? (there’s two but it’s okay if you know at least one)

A

Temporal validity; homosexuality used to be socially rejected and calssified as a mental health disorder, but as social norms changed it has been accepted. Inaccuracies in identification of mental health disorders/abnormalities.

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7
Q

(DoAbnormalities) What is DIMH?

A

Deviation from Ideal Mental Health suggested by jahoda, a criterion which must all be met by an individual to class them as healthy mentally speaking.

Criterion includes;

  • accurate perception of reality
  • resistance to stress
  • self-actualisation
  • autonomy
  • positive self-concept (congruence ig)
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8
Q

(DoAbnormalities) Disadvantage of DIMH?

A

Unrealisitc to suggest we must meet all the criteria presented, who can do that??

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9
Q

(DoAbnormalities) What is an advantage of DIMH?

A

It gives a practical checklisst that individuals may work on/clinicians may use to diagnose mental health disorders.

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10
Q

(DoAbnormalities) What is SI?

A

Statistical Infrequency: identifies abnormalities as the least prevalent characteristics/behaviours in society,

e.g. high and low IQ

uses two-tailed graph and either ends of spectrum to id abnormalities.

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11
Q

(DoAbnormalities) What’s an advantage of SI?

A

it’s highly objective and scientific; uses statistical data to calculate abnormalities.

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12
Q

(DoAbnormalities) Disadvantages of SI? (identify one or more pls)

A
  • Culturally dependent
  • Temporally dependent
  • Not always a bad infrequency
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13
Q

(Phobias) What is a phobia classed as in mental health terms?

A

An anxiety disorder

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14
Q

(Phobias) What are the 3 general symptoms of phobias? give examples for each.

A
  • Cognitive - less focus when around phobia
  • Emotional - Anxiety and Stress
  • Behavioural - Avoidance or Endurance w/ high levels of anxiety.
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15
Q

(Phobias) Who proposed the Two-Way Model?

A

Mowrer

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16
Q

(Phobias) What is the Two-Way Model?

A
  1. phobias first classically conditioned.
    1. stimulus generalisation.
  3. phobias reinforced with operant cond.
    1. avoidance learning used to cope.
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17
Q

(Phobias) What evidence was proposed by the theorist behind the TwoWay Model?

A

+ Mowrer taught rats avoidance learning shocks in rat cages; evidential of coping mechanism for a phobia.

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18
Q

(Phobias) What limitation arises from Mowrer’s research evidence?

A
  • Ethological evidence..
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19
Q

(Phobias) What’s bad about the approach the TwoWay Model is based on?
(what does it leave out completely)

A
  • Reductionist to leave out any biological implications of phobias, such as evolutionary advantage.
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20
Q

(Phobias) What application did the TwoWay Model lead to?

A

Implications for therapy; Systematic Desensitisation

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21
Q

(Sys.Desen) Detail Systematic Desensitisation

A
  1. Determine In Vitro/ In Vivo use.
  2. Relaxation techniques taught for counter conditioning.
  3. Anxiety Hierarchy determined.
  4. Gradual exposure to phobic stimuli.
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22
Q

(Sys.Desen) What did Klosko find?

A

+ 87% success rate of systematic desensitisation
33% unsuccessful rate.

differences significant enough to call sd effective.

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23
Q

(Sys.Desen) What technique used in SD provides a strength and why is it a strength?

A

+ impossible to feel relaxed and anxious at once; counter-conditioning technique of SD.

face validity of SD as a result, is strong

24
Q

(Sys.Desen) How was Klosko’s study flawed?

A
  • He looked at simple phobias, not all types so not v. generalisable.
25
Q

(Sys.Desen) Could phobias spring back after successful systematic desensitisation treatment? why?

A
  • doesn’t focus on the stem of phobia, only treating symptoms.
26
Q

(Flooding) Detail Flooding.

A
  1. in vivo, exposed to phobia directly.
  2. high levels of anxiety experienced.
  3. once realisation that life isn’t in danger, anxiety levels decrease (extinction - CC) and relaxation sets.
  4. phobia no longer associated with fear.
27
Q

(Flooding) Why is flooding convenient for patients?

A

+ Quicker and cheaper

28
Q

(Flooding) Why can flooding be bad for patients?

A
  • Can be extremely traumatic especially for children
29
Q

(Flooding) Is there evidence for flooding’s effectiveness?

A

+ Wolpe took girl out on a drive (she feared cars) and she was extremely distressed at first, but it wore off and she felt relaxed after a while.

No longer feared cars.

30
Q

(Flooding) What limitation of SD aligns with a limitation of flooding?

A

Both do not face the reason behind phobia, they only challenge symptoms.
Theorised that phobia may arise later on in life.

31
Q

(OCD intro) What kind of mental health disorder is OCD classed as?

A

OCD is classed as an anxiety disorder.

32
Q

(OCD intro) What are the three symptoms of OCD? Give an example for each.

A
  • Emotional characteristics: Disgust/Anxiety
  • Cognitive characteristics: Obsessive thoughts
  • Behavioural characteristics: Compulsive actions
33
Q

(OCD genetic) What is the genetic explanation of OCD?

A
  • OCD is likely to be an inherited disease.

- OCD is polygenic (Aetiologically heterogenous)

34
Q

(OCD genetic) What research support did Taylor present?

A

+ Taylor conducted meta-analysis found ~230 genetic variations linked to OCD. (this is what aetiologically heterogenous means, when a disorder has multiple genetic variations.)

35
Q

(OCD genetic) Why can we not rely solely on a genetic explanation?

A
  • Links have been made to suggest that the environment plays a role in expressings OCD (diathesis-stress model) so OCD is not solely genetic based.
36
Q

(OCD genetic) Miguel conducted twin studies. What were his findings and are they strengths or limitations for OCD?

A

Concordance rates were roughly halved in DZ for MZ.
Suggests that genetic influence is correct, because MZ share 100% and DZ share 50% so prevalence should be half as likely in DZ as it is for MZ.

37
Q

(OCD genetic) What did Lewis find to support genetic explanations of OCD?

A

+ 37% of OCD sufferers have a parent with OCD

+ 21% of OCD sufferers have siblings with OCD.

38
Q

(OCD neural) Briefly outline the two neural explanations of OCD.

A

one explanation is that the levels of serotonin determine whether an individual is likely to have OCD or not.
abnormally low levels linked to:
- low mood levels
- repetition of tasks

other explanations is that the brain structure determines whether an individual is likely to have OCD or not.

39
Q

(OCD brain) What is the role of the OFC and how is it different in OCD ppl?

A

OFC integrates sensory info, makes decisions, and anticipates rewards/punishments.
OFC detects imaginary errors and sends worry signal to Caudate Nucleus.

40
Q

(OCD brain) What is the role of the Caudate Nucleus and how is it different in OCD ppl?

A

Caudate Nucleus processes unwanted/irrelevant thoughts.

OCD brain does not do this, signal sent along to thalamus.

41
Q

(OCD brain) What is the role of the thalamus and how is it different in OCD ppl?

A

Thalamus controls motor and thinking functions.
OCD brain produces repetitive actions in response to worry signals.
Signal that error has been fixed controls the Cingulate Gyrus’ emotional response.

42
Q

(OCD brain) What is the role of the Cingulate Gyrus and what does it do in OCD ppl?

A

Produces emotional responses.

OCD brain, produces feelings of disgust/anxiety.

43
Q

(OCD brain) How are all of these neural systems linked?

A

Overactive OFC sends worry signals through Caudate Nucleus which doesn’t filter them out as irrelevant, so the Thalamus produces a motor response to suppress worry signal and resolve the emotional response of the Cingulate Gyrus.

44
Q

(OCD brain) What objective research evidence did Paul provide to support brain systems’ involvement in OCD?

A

+ showed that there was a high activation of the OFC in OCD brains.

45
Q

(OCD brain) What argument can be proposed for the brain structure explanation?

A

Were the abnormal brain structures a cause or effect of OCD?

46
Q

(OCD NTM) Hu provided research support for the serotonin explanation?

A

Hu found that in 66.8% of OCD ppts. levels of serotonin were abnormally low.

47
Q

(OCD NTM) What argument can be used against levels of serotonin in the brain and its direct relation with OCD?

A

Well, 2/3 OCD sufferers have depression
(CO-MORBIDITY).
Depression linked with low levels of serotonin.
Depression or OCD which is causing the low levels in an OCD sufferer??

48
Q

(OCD Therapy) Briefly detail drug therapy for OCD.

A
  1. Use of antidepressants such as SSRIs or Tricyclics to increase levels of serotonin available for uptake by postsynaptic membrane receptors.
  2. Idea is to combat the low levels of serotonin to decrease symptoms of OCD such as repetitive tasks (compulsions)
49
Q

(OCD Therapy) What are SSRIs?

A

Selective Serotonin Reuptake Inhibitors:

block the reuptake of serotonin, leaving more available (in the cleft) for synaptic transmission.

50
Q

(OCD Therapy) How long do SSRIs take to work?

A

Roughly 4 months.

51
Q

(OCD Therapy) What are Tricyclics?

A

Tricyclics, first type of antidepressant used against OCD, are less selective than SSRIs.
Block both serotonin AND noradrenaline reuptake by presynaptic membrane, making more available for uptake in transmission.
Have more severe symptoms.

52
Q

(OCD Therapy) Examples of SSRIs and Tricyclics?

A

Anafran (Tricyclic)

Prozac (SSRI)

53
Q

(OCD Therapy) Name some symptoms of SSRIs.

A
  • Symptoms may include nausea, loss of sex drive
54
Q

(OCD Therapy) Name some symptoms of Tricyclics/SRIs.

A
  • more severe; hallucinations, weight gain or increased heart rate.
55
Q

(OCD Therapy) How are symptoms related to effectiveness of Drug Therapy?

A

Well, SSRI’s don’t have severe symptoms, but if they don’t work then Tricyclics are used and they have much worse symptoms.

These symptoms may put someone off using their medication, indirectly reducing the effectiveness of Drug Therapy.

56
Q

(OCD Therapy) Why are drugs preferred by both the NHS and convenient for the Individual?

A

+ Cheaper for NHS than CBT.
+ Takes less time than CBT.

(Two separate evaluations)

57
Q

(OCD Therapy) Simpson said Drug therapy is limited in what way?

A
  • He said they’re a short term fix.

- Research support suggested 45% of OCD sufferers using drug therapy relapsed within 12 weeks.

AQA Psychology (A Level) (9 decks)

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