Psychopathology
Definitions of Abnormality
Characteristics of phobias
The Behavioural Approach to Explaining Phobias
The Behavioural approach to treating phobias
Characteristics of depression
Cognitive Approach to Explaining Depression
Cognitive Approach to Treating Depression
OCD Characteristics
Biological explanations of OCD
Biological treatment of OCD
Biological treatment of OCD
A01 Serotonin is implicated in the ‘worry circuit’, increasing levels may normalise this. SSRIs e.g Prozac and
Zoloft work with serotonin, reducing anxiety as serotonin has inhibitory effect on postsynaptic neurons. An
increase of serotonin in the synapse has SSRIS blocking the transporter mechanism reabsorbing serotonin into
the presynaptic neuron after firing. More serotonin is left in the synapse, prolonging its activity, relieving anxiety
symptoms.
A01 Tricyclics treat OCD as a block transporter mechanism reabsorbing serotonin and noradrenaline into
presynaptic cells after firing. These neurotransmitters are left in the synapse, prolonging the activity and easing
transmission of the next impulse. Tricyclics have the advantage of targeting more than one neurotransmitter,
usually the second line treatment as loads of side effects.
A01 BZs anti anxiety medication. Increases the effect of neurotransmitter GABA which has an inhibitory effect -
tells neurons to stop stressing. When GABA locks into the receptor site, the flow of chloride ions into the neuron
is increased. Chloride ions make it more difficult for the receiving neuron to be stimulated by further
neurotransmitters. Nervous system slowed down so the patient was more relaxed. When a BZ is added and
binded to receptor sites, the process is enhanced, more chloride ions, negative charge so less fire.
A03 Soomro et al reviewed studies of SSRIs with OCD patients finding them more effective than placebos in
reducing symptoms of OCD up to 3 months after treatment. 70% patients had less symptoms. Not effective with
everybody
A03 Maina et al found patients relapsed within a few weeks if their medication stopped. This only temporarily
raises the levels, relieving symptoms, it doesn’t solve the issue. Combo better as not long term - interactionist
A03 Drug therapies less time effort and cheap and little monitoring vs cbt thought effort
A03 Side effects of SSRIs: nausea, headaches, insomnia (Soomro). Tricyclic more side effects e.g hallucinations
or irregular heartbeat so only used when SSRi ineffective. BZs side effects - aggressiveness, long term
impairment in memory. addiction , dosage should be limited (Ashton).
Biological explanations of OCD
A01 Genetic - inherited genes. Lewis - 37% of patients with OCD had parents with disorder. Nestadt - first
degree relatives with OCD 5x more likely to have illness.
OCD polygenic - several candidate genes involved e.g Taylor - 230 genes found.
COMT gene = high level dopamine. SERT gene = lower levels of serotonin.
Aetiological heterogeneity – different combinations of genes may cause OCD in different people
Neural structures - Genetic predispositions may affect brain structure. The orbitofrontal cortex sends worry
signals to the thalamus. These are normally suppressed by the caudate nucleus but if damaged it fails to
suppress minor worry signals and the thalamus is continually alerted confirming the worry to the OFC and
creating a worry signal. Supported by PET scans showing heightened activity in the OFC when symptoms are
active.
A01 Neural - Low serotonin - regulating mood, if this transmission does not take place as normal, mood, and
other mental processes such as anxiety, can also be affected. Comer - serotonin plays a key role in the operation
of the OFC and the caudate nuclei, and low levels might be the cause of malfunction in this area.
, A03 Billet et al found in a meta analysis that MZ twins were twice as likely to develop OCD if their cotwin had the
disorder versus DZ twins. MZ shares 100% genetics. Concordance rates are never 100% meaning environmental
factors play a role too, genetics alone cant account for all OCD cases.
A03 Nature versus nurture/ reductionist - ignores the role of nurture, found trauma triggers OCD, not just
genetics. Genetics create a biological predisposition to the disorder so more vulnerable to developing. Trauma
acts as a stressor triggering the disorder which affects the treatment of OCD - more psychological treatments.
A03 support for neural explanations of OCD come from research for biological treatments of OCD.
Antidepressants work by increasing neurotransmitter serotonin. These are effective in reducing symptoms of
OCD and provide support for a neural explanation of OCD.
A03 Comorbidity - OCD patients are depressed often, depression is caused by a disruption to the serotonin
system with low levels.
OCD Characteristics
Behavioural characteristics - compulsions and avoidance
Emotional - anxiety and stress
Cognitive - obsessive thoughts and insight into excessive anxiety
Cognitive approach and treating depression
A01) Challenging irrational beliefs using Ellis ABCDEF. Activating events, beliefs about activating events and
consequences challenged by disputing, effective attitude to life, new feelings produced. Logical disputing (make
sense), empirical disputing (evidence for or against), pragmatic disputing (likely going to help). Effective disputing
changes self defeating beliefs into rational.
A01) Clients are asked to complete assignments testing irrational beliefs against reality and replacing them with
rational beliefs. Behavioural action requires more activeness and pleasurable activities, respect and appreciation
regardless of the clients efforts (unconditional positive regard). This facilitates cognitive and behavioural changes.
A03) March et al did a 36 week treatment on adolescents, 81% positive treatment with CBT, 81% positive
antidepressant group, and 86% combination significantly improved. CBT is just as successful as public health
alongside medication. CBT 1st choice in NHS, less side effects of drug therapies.
A03) Babyak et al found adults significantly improved at the end of 4 months with either drugs, exercise or
combination. 6 months later the exercise groups had lower relapse rates. Superhero activation creates a habit
and a structure so one is more active. This means less money is spent on treatment and time off work on
benefits, no taxes so better for the economy.
A03) May not be applicable with challenging circumstances, this minimises the importance of circumstances
where a patient may be living in e.g poverty, abuse, death, which may demotivate people as a hindrance.
A03) This may not work for those with severe depression as one cannot motivate themselves as they have no
attention in session so either won’t go to the session or do the homework. Antidepressants may be better to start
with, then CBT later when one is more alert and motivated.
Cognitive approach to explaining depression
A01 Ellis suggested irrational thoughts are a way of explaining depression. This can be seen in his ABC model (A
= activating event, B =beliefs (musterbation (always achieve perfection), utopianism (life is always meant to be
fair) and i-can't-stand-it-itis (major disaster when things don't go smoothly) C = consequences=
A01 Beck suggested it was due to cognitions and faulty processing when one focuses only on the negatives with
black-and-white thinking, blowing small problems. These are based on negative schemas which act as a mental
framework/template, This is based on a self schema with a dysfunctional view of the world, self and future
(negative triad)
A03 Bates et al studied depressed participants and gave them negative automatic thought statements and they
became more and more depressed. This supports irrational thinking as negative thoughts cause depression or
vice versa. Genetic vulnerability causes faulty thinking.
A03 RWA CBT for treatments of depression which challenges irrational beliefs through Ellis’s model. Clients
asked to complete homework tasks.
Definitions of Abnormality
Characteristics of phobias
The Behavioural Approach to Explaining Phobias
The Behavioural approach to treating phobias
Characteristics of depression
Cognitive Approach to Explaining Depression
Cognitive Approach to Treating Depression
OCD Characteristics
Biological explanations of OCD
Biological treatment of OCD
Biological treatment of OCD
A01 Serotonin is implicated in the ‘worry circuit’, increasing levels may normalise this. SSRIs e.g Prozac and
Zoloft work with serotonin, reducing anxiety as serotonin has inhibitory effect on postsynaptic neurons. An
increase of serotonin in the synapse has SSRIS blocking the transporter mechanism reabsorbing serotonin into
the presynaptic neuron after firing. More serotonin is left in the synapse, prolonging its activity, relieving anxiety
symptoms.
A01 Tricyclics treat OCD as a block transporter mechanism reabsorbing serotonin and noradrenaline into
presynaptic cells after firing. These neurotransmitters are left in the synapse, prolonging the activity and easing
transmission of the next impulse. Tricyclics have the advantage of targeting more than one neurotransmitter,
usually the second line treatment as loads of side effects.
A01 BZs anti anxiety medication. Increases the effect of neurotransmitter GABA which has an inhibitory effect -
tells neurons to stop stressing. When GABA locks into the receptor site, the flow of chloride ions into the neuron
is increased. Chloride ions make it more difficult for the receiving neuron to be stimulated by further
neurotransmitters. Nervous system slowed down so the patient was more relaxed. When a BZ is added and
binded to receptor sites, the process is enhanced, more chloride ions, negative charge so less fire.
A03 Soomro et al reviewed studies of SSRIs with OCD patients finding them more effective than placebos in
reducing symptoms of OCD up to 3 months after treatment. 70% patients had less symptoms. Not effective with
everybody
A03 Maina et al found patients relapsed within a few weeks if their medication stopped. This only temporarily
raises the levels, relieving symptoms, it doesn’t solve the issue. Combo better as not long term - interactionist
A03 Drug therapies less time effort and cheap and little monitoring vs cbt thought effort
A03 Side effects of SSRIs: nausea, headaches, insomnia (Soomro). Tricyclic more side effects e.g hallucinations
or irregular heartbeat so only used when SSRi ineffective. BZs side effects - aggressiveness, long term
impairment in memory. addiction , dosage should be limited (Ashton).
Biological explanations of OCD
A01 Genetic - inherited genes. Lewis - 37% of patients with OCD had parents with disorder. Nestadt - first
degree relatives with OCD 5x more likely to have illness.
OCD polygenic - several candidate genes involved e.g Taylor - 230 genes found.
COMT gene = high level dopamine. SERT gene = lower levels of serotonin.
Aetiological heterogeneity – different combinations of genes may cause OCD in different people
Neural structures - Genetic predispositions may affect brain structure. The orbitofrontal cortex sends worry
signals to the thalamus. These are normally suppressed by the caudate nucleus but if damaged it fails to
suppress minor worry signals and the thalamus is continually alerted confirming the worry to the OFC and
creating a worry signal. Supported by PET scans showing heightened activity in the OFC when symptoms are
active.
A01 Neural - Low serotonin - regulating mood, if this transmission does not take place as normal, mood, and
other mental processes such as anxiety, can also be affected. Comer - serotonin plays a key role in the operation
of the OFC and the caudate nuclei, and low levels might be the cause of malfunction in this area.
, A03 Billet et al found in a meta analysis that MZ twins were twice as likely to develop OCD if their cotwin had the
disorder versus DZ twins. MZ shares 100% genetics. Concordance rates are never 100% meaning environmental
factors play a role too, genetics alone cant account for all OCD cases.
A03 Nature versus nurture/ reductionist - ignores the role of nurture, found trauma triggers OCD, not just
genetics. Genetics create a biological predisposition to the disorder so more vulnerable to developing. Trauma
acts as a stressor triggering the disorder which affects the treatment of OCD - more psychological treatments.
A03 support for neural explanations of OCD come from research for biological treatments of OCD.
Antidepressants work by increasing neurotransmitter serotonin. These are effective in reducing symptoms of
OCD and provide support for a neural explanation of OCD.
A03 Comorbidity - OCD patients are depressed often, depression is caused by a disruption to the serotonin
system with low levels.
OCD Characteristics
Behavioural characteristics - compulsions and avoidance
Emotional - anxiety and stress
Cognitive - obsessive thoughts and insight into excessive anxiety
Cognitive approach and treating depression
A01) Challenging irrational beliefs using Ellis ABCDEF. Activating events, beliefs about activating events and
consequences challenged by disputing, effective attitude to life, new feelings produced. Logical disputing (make
sense), empirical disputing (evidence for or against), pragmatic disputing (likely going to help). Effective disputing
changes self defeating beliefs into rational.
A01) Clients are asked to complete assignments testing irrational beliefs against reality and replacing them with
rational beliefs. Behavioural action requires more activeness and pleasurable activities, respect and appreciation
regardless of the clients efforts (unconditional positive regard). This facilitates cognitive and behavioural changes.
A03) March et al did a 36 week treatment on adolescents, 81% positive treatment with CBT, 81% positive
antidepressant group, and 86% combination significantly improved. CBT is just as successful as public health
alongside medication. CBT 1st choice in NHS, less side effects of drug therapies.
A03) Babyak et al found adults significantly improved at the end of 4 months with either drugs, exercise or
combination. 6 months later the exercise groups had lower relapse rates. Superhero activation creates a habit
and a structure so one is more active. This means less money is spent on treatment and time off work on
benefits, no taxes so better for the economy.
A03) May not be applicable with challenging circumstances, this minimises the importance of circumstances
where a patient may be living in e.g poverty, abuse, death, which may demotivate people as a hindrance.
A03) This may not work for those with severe depression as one cannot motivate themselves as they have no
attention in session so either won’t go to the session or do the homework. Antidepressants may be better to start
with, then CBT later when one is more alert and motivated.
Cognitive approach to explaining depression
A01 Ellis suggested irrational thoughts are a way of explaining depression. This can be seen in his ABC model (A
= activating event, B =beliefs (musterbation (always achieve perfection), utopianism (life is always meant to be
fair) and i-can't-stand-it-itis (major disaster when things don't go smoothly) C = consequences=
A01 Beck suggested it was due to cognitions and faulty processing when one focuses only on the negatives with
black-and-white thinking, blowing small problems. These are based on negative schemas which act as a mental
framework/template, This is based on a self schema with a dysfunctional view of the world, self and future
(negative triad)
A03 Bates et al studied depressed participants and gave them negative automatic thought statements and they
became more and more depressed. This supports irrational thinking as negative thoughts cause depression or
vice versa. Genetic vulnerability causes faulty thinking.
A03 RWA CBT for treatments of depression which challenges irrational beliefs through Ellis’s model. Clients
asked to complete homework tasks.
