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subcortical pathways, particularly the mesolimbic pathway, is associated with positive symptoms such as hallucinations and delusions."},{"text":"negative symptoms","correct":false,"explanation":"Negative symptoms are associated with reduced dopamine activity in the prefrontal cortex. Subcortical hyperdopaminergia instead produces positive symptoms such as hallucinations."},{"text":"cognitive symptoms","correct":false,"explanation":"Cognitive difficulties are more closely associated with dysfunction in cortical regions. Excess subcortical dopamine is specifically linked to positive symptoms such as hallucinations and delusions."},{"text":"depressive symptoms","correct":false,"explanation":"Depressive symptoms are not the symptom category explained by subcortical hyperdopaminergia. The dopamine hypothesis links this excess activity to positive symptoms such as hallucinations."}]},{"id":"b8c80f1e-76ff-43d7-8329-a53cce965dbc","cardType":"basic","points":1,"front":"According to the dopamine hypothesis, hypodopaminergia in the prefrontal cortex causes which symptom type?","back":"Negative symptoms, such as avolition.","mcqOptions":[{"text":"Negative symptoms, such as avolition.","correct":true,"explanation":"Reduced dopamine activity in the prefrontal cortex, particularly in the mesocortical pathway, is associated with negative symptoms such as avolition and reduced speech."},{"text":"Positive symptoms, such as hallucinations.","correct":false,"explanation":"Positive symptoms are linked to excessive dopamine activity in subcortical areas, not reduced prefrontal activity. Prefrontal hypodopaminergia causes negative symptoms such as avolition."},{"text":"Extrapyramidal symptoms, such as tremors.","correct":false,"explanation":"Extrapyramidal symptoms are motor side effects caused by dopamine blockade in the nigrostriatal pathway. Prefrontal hypodopaminergia instead explains negative symptoms such as avolition."},{"text":"Mood symptoms, such as mania.","correct":false,"explanation":"Mania is not the symptom type attributed to reduced prefrontal dopamine in schizophrenia. The dopamine hypothesis links this reduction to negative symptoms such as avolition."}]},{"id":"a8d2296a-e373-4583-8dbf-d279f481b574","cardType":"cloze","points":null,"front":"Typical antipsychotics reduce dopamine neurotransmission by acting as [ ] at D₂ receptors.","back":"Typical antipsychotics reduce dopamine neurotransmission by acting as dopamine antagonists at D₂ receptors.","mcqOptions":[{"text":"dopamine antagonists","correct":true,"explanation":"Typical antipsychotics occupy D₂ receptors without activating them, blocking dopamine’s effects and reducing the excessive neurotransmission associated with positive symptoms."},{"text":"dopamine agonists","correct":false,"explanation":"Agonists activate dopamine receptors and would increase rather than reduce dopamine signalling. Typical antipsychotics are dopamine antagonists that block D₂ receptors."},{"text":"partial dopamine agonists","correct":false,"explanation":"Partial agonism is associated with some newer antipsychotics rather than typical drugs. Typical antipsychotics act as dopamine antagonists, preventing D₂ receptor activation."},{"text":"dopamine reuptake inhibitors","correct":false,"explanation":"Reuptake inhibitors leave more dopamine in the synapse and therefore increase its effects. Typical antipsychotics reduce transmission by acting as dopamine antagonists at D₂ receptors."}]},{"id":"7dcf182a-fce2-46c2-9f17-dd6f1f595783","cardType":"basic","points":2,"front":"How does atypical D₂ binding differ from typical antipsychotic binding?","back":"Atypicals bind temporarily and dissociate rapidly.","mcqOptions":[{"text":"Atypicals bind temporarily and dissociate rapidly.","correct":true,"explanation":"Atypical antipsychotics occupy D₂ receptors briefly and detach quickly, allowing more normal dopamine transmission and reducing the risk of severe motor side effects."},{"text":"Atypicals bind permanently and do not dissociate.","correct":false,"explanation":"Antipsychotic binding is reversible rather than permanent. Atypicals characteristically bind temporarily and dissociate rapidly from D₂ receptors, unlike the more sustained binding of typical drugs."},{"text":"Atypicals bind strongly and dissociate slowly.","correct":false,"explanation":"Slow dissociation describes the more sustained D₂ blockade associated with typical antipsychotics. Atypicals bind temporarily and dissociate rapidly, helping to limit motor side effects."},{"text":"Atypicals bind indirectly and increase receptor sensitivity.","correct":false,"explanation":"Atypicals act directly at D₂ receptors rather than increasing their sensitivity. Their distinguishing pattern is temporary binding followed by rapid dissociation."}]},{"id":"66afec3c-f57f-45e5-908b-18a323a895bd","cardType":"cloze","points":null,"front":"Atypical antipsychotics also block serotonin [ ] receptors.","back":"Atypical antipsychotics also block serotonin 5-HT2A receptors.","mcqOptions":[{"text":"5-HT2A","correct":true,"explanation":"Atypical antipsychotics block serotonin 5-HT2A receptors as well as dopamine D₂ receptors, contributing to their effects on negative symptoms and reduced motor side effects."},{"text":"5-HT1B","correct":false,"explanation":"5-HT1B is a different serotonin receptor subtype and is not the key target identified in the standard explanation of atypical antipsychotics. The relevant receptor is 5-HT2A."},{"text":"5-HT3","correct":false,"explanation":"5-HT3 receptors are best known for their role in nausea and vomiting. Atypical antipsychotic action is characteristically associated with blockade of serotonin 5-HT2A receptors."},{"text":"5-HT4","correct":false,"explanation":"5-HT4 receptors are associated mainly with gastrointestinal and cognitive functions, not the defining serotonin action of atypical antipsychotics. These drugs characteristically block 5-HT2A receptors."}]},{"id":"b7096fae-0dd7-43e9-aaf4-70cf51eaef76","cardType":"basic","points":1,"front":"Which severe motor side effect involves uncontrollable grimacing and blinking?","back":"Tardive dyskinesia.","mcqOptions":[{"text":"Tardive dyskinesia.","correct":true,"explanation":"Tardive dyskinesia is a severe, potentially irreversible motor disorder involving involuntary facial movements, including grimacing, blinking and tongue movements."},{"text":"Parkinsonism.","correct":false,"explanation":"Parkinsonism usually produces tremor, muscular rigidity and slowed movement rather than repetitive facial movements. Uncontrollable grimacing and blinking indicate tardive dyskinesia."},{"text":"Akathisia.","correct":false,"explanation":"Akathisia causes intense restlessness and an inability to remain still. Repetitive involuntary facial movements such as grimacing and blinking are characteristic of tardive dyskinesia."},{"text":"Neuroleptic malignant syndrome.","correct":false,"explanation":"Neuroleptic malignant syndrome involves fever, severe rigidity and autonomic instability and is a medical emergency. Uncontrollable grimacing and blinking instead indicate tardive dyskinesia."}]},{"id":"0a407cda-5317-4b8c-8a63-56fc4300bbe1","cardType":"basic","points":1,"front":"Why do patients taking Clozapine need regular blood tests?","back":"Risk of agranulocytosis, a life-threatening white blood cell drop.","mcqOptions":[{"text":"Risk of agranulocytosis, a life-threatening white blood cell drop.","correct":true,"explanation":"Clozapine can dangerously suppress white blood cell production, weakening immune defence. Regular blood tests monitor cell counts so agranulocytosis can be detected early."},{"text":"Risk of leukocytosis, a life-threatening white blood cell rise.","correct":false,"explanation":"This reverses the direction of the relevant blood-cell change. Clozapine monitoring is required because agranulocytosis causes a dangerous drop in white blood cells."},{"text":"Risk of anaemia, a life-threatening red blood cell drop.","correct":false,"explanation":"Anaemia concerns red blood cells and is not the key reason for mandatory Clozapine blood monitoring. The specific risk is agranulocytosis, a severe white blood cell drop."},{"text":"Risk of thrombocytopenia, a life-threatening platelet drop.","correct":false,"explanation":"Thrombocytopenia affects platelets and blood clotting rather than the immune cells primarily monitored during Clozapine treatment. Testing targets agranulocytosis, a dangerous white blood cell drop."}]},{"id":"45cb8d93-e764-4c1d-a3e3-3978b3104d37","cardType":"basic","points":2,"front":"What did Thornley et al. (2003) find when comparing Chlorpromazine with placebo?","back":"

Better overall functioning with Chlorpromazine.
Reduced symptom severity with Chlorpromazine.

","mcqOptions":[{"text":"

Better overall functioning with Chlorpromazine.
Reduced symptom severity with Chlorpromazine.

","correct":true,"explanation":"Thornley et al. found that Chlorpromazine produced better overall functioning and reduced symptom severity compared with placebo, supporting its effectiveness in treating schizophrenia."},{"text":"

Worse overall functioning with Chlorpromazine.
Reduced symptom severity with Chlorpromazine.

","correct":false,"explanation":"The symptom finding is accurate, but the functioning result has been reversed. Chlorpromazine was associated with better overall functioning as well as reduced symptom severity."},{"text":"

Better overall functioning with Chlorpromazine.
Increased symptom severity with Chlorpromazine.

","correct":false,"explanation":"The functioning finding is accurate, but Chlorpromazine did not increase symptom severity. Thornley et al. found reduced symptom severity alongside better overall functioning."},{"text":"

No difference in functioning with Chlorpromazine.
No difference in symptoms with Chlorpromazine.

","correct":false,"explanation":"The review did not find Chlorpromazine equivalent to placebo on both outcomes. It was associated with better overall functioning and reduced symptom severity."}]},{"id":"6e696cd8-51e4-4655-ae63-297fbbed1e48","cardType":"basic","points":2,"front":"What is the chemical straitjacket criticism of antipsychotics?","back":"

Used to calm/manage patients for staff convenience.
Raises autonomy and consent concerns.

","mcqOptions":[{"text":"

Used to calm/manage patients for staff convenience.
Raises autonomy and consent concerns.

","correct":true,"explanation":"The criticism is that antipsychotics may be used primarily to make patients easier for staff to manage. This can restrict patient autonomy, especially where consent is limited or absent."},{"text":"

Used to increase/restore patients’ cognitive abilities.
Raises memory and intelligence concerns.

","correct":false,"explanation":"This confuses behavioural control with cognitive enhancement. The chemical straitjacket criticism concerns using medication to calm or manage patients for staff convenience, creating autonomy and consent concerns."},{"text":"

Used to diagnose/classify patients through drug response.
Raises reliability and validity concerns.

","correct":false,"explanation":"Using treatment response to classify disorders is not the chemical straitjacket criticism. The criticism is that drugs may control patients for staff convenience, compromising autonomy and meaningful consent."},{"text":"

Used to punish/deter patients for disruptive behaviour.
Raises conditioning and relapse concerns.

","correct":false,"explanation":"The criticism does not define antipsychotics as behavioural punishments. It focuses on their use to calm or manage patients for staff convenience and the resulting autonomy and consent issues."}]},{"id":"2b22f9e0-251d-46df-94a9-4a75de91ed60","cardType":"basic","points":1,"front":"When CBTp treats hallucinations or delusions, what is it mainly trying to reduce?","back":"The distress they cause, not the experiences themselves.","mcqOptions":[{"text":"The distress they cause, not the experiences themselves.","correct":true,"explanation":"CBTp does not necessarily eliminate hallucinations or delusions. It primarily changes how patients interpret and respond to these experiences, reducing the distress and disruption associated with them."},{"text":"The frequency of them, until the experiences disappear completely.","correct":false,"explanation":"Expecting CBTp to remove psychotic experiences completely confuses symptom elimination with psychological coping. Its main aim is to reduce the distress caused by hallucinations or delusions."},{"text":"The medication they require, not the distress they produce.","correct":false,"explanation":"Reducing medication is not the main target when CBTp addresses hallucinations or delusions. Therapy chiefly helps patients reinterpret the experiences so that they cause less distress."},{"text":"The evidence supporting them, until patients deny the experiences.","correct":false,"explanation":"CBTp evaluates beliefs without pressuring patients simply to deny their experiences. Its central aim is to reduce the distress those hallucinations or delusions cause, rather than erase them."}]},{"id":"5e4cad9a-9591-4c00-b34a-39afe6de1c7f","cardType":"basic","points":2,"front":"In CBTp, what is the purpose of formulation?","back":"Create a collaborative picture of experiences, triggers and feelings.","mcqOptions":[{"text":"Create a collaborative picture of experiences, triggers and feelings.","correct":true,"explanation":"Formulation brings therapist and patient together to identify how experiences, triggers, thoughts and feelings connect. This shared understanding guides therapy and makes treatment personally relevant."},{"text":"Create a clinical diagnosis from symptoms, duration and severity.","correct":false,"explanation":"A formulation is not primarily a diagnostic label based on symptom criteria. It creates a collaborative picture of the patient’s experiences, triggers and feelings to guide therapy."},{"text":"Create a fixed therapist judgement of irrational beliefs and behaviours.","correct":false,"explanation":"Formulation should not be a judgement imposed solely by the therapist. It is a collaborative picture developed with the patient, linking their experiences, triggers and feelings."},{"text":"Create a standard symptom checklist of hallucinations, delusions and speech.","correct":false,"explanation":"A symptom checklist records features but does not provide an individual formulation. Formulation collaboratively connects the patient’s experiences with relevant triggers and feelings to inform treatment."}]},{"id":"246ecf89-3aaa-4db5-a2a1-c5375fa421c6","cardType":"basic","points":2,"front":"How does normalisation help in CBTp?","back":"Explains voice-hearing can occur under extreme stress, reducing alienation.","mcqOptions":[{"text":"Explains voice-hearing can occur under extreme stress, reducing alienation.","correct":true,"explanation":"Normalisation presents voice-hearing as an experience that can occur during extreme stress, rather than something uniquely abnormal. This helps patients feel less isolated or alienated."},{"text":"Explains voice-hearing results from personal weakness, reducing uncertainty.","correct":false,"explanation":"Attributing voices to personal weakness would increase blame and alienation rather than normalise the experience. CBTp explains that voice-hearing can occur under extreme stress."},{"text":"Explains voice-hearing proves an external presence, reducing doubt.","correct":false,"explanation":"Confirming that voices come from an external presence could reinforce a delusional interpretation. Normalisation instead explains that voice-hearing can occur under extreme stress, reducing alienation."},{"text":"Explains voice-hearing requires social withdrawal, reducing stimulation.","correct":false,"explanation":"Encouraging withdrawal may worsen isolation and does not constitute normalisation. Normalisation explains that voice-hearing can occur under extreme stress, helping the patient feel less alienated."}]},{"id":"245c73a0-0ded-43fe-9717-e0ab3f8fcad1","cardType":"cloze","points":null,"front":"CBTp uses [ ] to encourage patients to evaluate delusional logic.","back":"CBTp uses Socratic questioning to encourage patients to evaluate delusional logic.","mcqOptions":[{"text":"Socratic questioning","correct":true,"explanation":"Socratic questioning uses carefully structured questions to help patients examine the evidence and logic behind delusional beliefs, without the therapist directly confronting or dismissing them."},{"text":"systematic desensitisation","correct":false,"explanation":"Systematic desensitisation treats phobic anxiety through relaxation and gradual exposure, rather than evaluating delusional logic. CBTp uses Socratic questioning to examine evidence and alternative interpretations."},{"text":"free association","correct":false,"explanation":"Free association is a psychodynamic technique in which thoughts are expressed without censorship. CBTp instead uses Socratic questioning to help patients evaluate the logic and evidence behind delusions."},{"text":"aversion therapy","correct":false,"explanation":"Aversion therapy pairs unwanted behaviour with an unpleasant stimulus and is not a method for examining beliefs. CBTp uses Socratic questioning to evaluate delusional logic collaboratively."}]},{"id":"f8f3dcb6-a218-434a-86d7-3241cd936721","cardType":"basic","points":2,"front":"Why may severe negative symptoms make CBTp unsuitable?","back":"CBTp requires effort, insight and motivation to engage.","mcqOptions":[{"text":"CBTp requires effort, insight and motivation to engage.","correct":true,"explanation":"Severe negative symptoms such as avolition and reduced emotional engagement can undermine the effort, insight and motivation needed to participate actively in CBTp tasks and discussion."},{"text":"CBTp requires sedation, compliance and supervision to engage.","correct":false,"explanation":"These requirements relate more closely to medication management than psychological therapy. CBTp depends on the patient having sufficient effort, insight and motivation to participate actively."},{"text":"CBTp requires strong memory and high intelligence to engage.","correct":false,"explanation":"CBTp does not require unusually high intelligence or exceptionally strong memory. The relevant difficulty is that severe negative symptoms reduce the effort, insight and motivation needed for engagement."},{"text":"CBTp requires hallucinations, delusions and paranoia to engage.","correct":false,"explanation":"These positive symptoms may be treatment targets, but they are not engagement requirements. CBTp needs effort, insight and motivation, which severe negative symptoms can substantially reduce."}]},{"id":"69642523-80ee-4927-9d6d-fa8c2100c425","cardType":"cloze","points":null,"front":"Unipolar depression is linked to low levels of [ ] in mood-regulating neural networks.","back":"Unipolar depression is linked to low levels of serotonin in mood-regulating neural networks.","mcqOptions":[{"text":"serotonin","correct":true,"explanation":"The monoamine explanation associates unipolar depression with reduced serotonin activity in neural networks involved in regulating mood, although depression is not explained by one neurotransmitter alone."},{"text":"adrenaline","correct":false,"explanation":"Adrenaline primarily supports physiological arousal and the fight-or-flight response, rather than being the neurotransmitter identified here. The standard account links unipolar depression with low serotonin."},{"text":"melatonin","correct":false,"explanation":"Melatonin regulates sleep-wake cycles, so disrupted levels may affect sleep in depression, but it is not the intended mood-network transmitter. The correct term is serotonin."},{"text":"acetylcholine","correct":false,"explanation":"Acetylcholine is strongly associated with muscle activation, attention and memory rather than the standard monoamine account given here. Unipolar depression is linked to low serotonin levels."}]},{"id":"09585659-2189-4b05-a6fc-8e9eb83663fe","cardType":"cloze","points":null,"front":"SSRIs increase synaptic serotonin by blocking serotonin [ ] transporters.","back":"SSRIs increase synaptic serotonin by blocking serotonin reuptake transporters.","mcqOptions":[{"text":"reuptake","correct":true,"explanation":"SSRIs block serotonin reuptake transporters, preventing serotonin from being rapidly reabsorbed into the presynaptic neuron. This leaves more serotonin available in the synaptic cleft."},{"text":"release","correct":false,"explanation":"Blocking serotonin release would reduce the amount entering the synapse, opposing the intended effect of SSRIs. They block reuptake transporters so serotonin remains in the synaptic cleft longer."},{"text":"synthesis","correct":false,"explanation":"SSRIs do not work by blocking the production of serotonin, which would tend to reduce its availability. They inhibit reuptake transporters and increase serotonin within the synapse."},{"text":"degradation","correct":false,"explanation":"Blocking neurotransmitter degradation describes the action of enzyme inhibitors such as MAOIs, not SSRIs. SSRIs specifically block serotonin reuptake transporters, increasing synaptic serotonin availability."}]},{"id":"06fec257-85d1-4394-b470-3ab7a2377c0a","cardType":"basic","points":2,"front":"What happens to serotonin after SSRIs block reuptake?","back":"

Remains longer in the synaptic cleft.
Repeatedly activates post-synaptic receptors.

","mcqOptions":[{"text":"

Remains longer in the synaptic cleft.
Repeatedly activates post-synaptic receptors.

","correct":true,"explanation":"SSRIs prevent serotonin from being transported back into the presynaptic neuron. It therefore remains available in the synapse and continues stimulating post-synaptic receptors."},{"text":"

Is immediately broken down in the synaptic cleft.
Stops activating post-synaptic receptors.

","correct":false,"explanation":"Blocking reuptake does not cause immediate serotonin breakdown or stop receptor activity. Serotonin remains longer in the synaptic cleft and repeatedly activates post-synaptic receptors."},{"text":"

Returns more quickly to the presynaptic neuron.
Repeatedly activates presynaptic receptors.

","correct":false,"explanation":"This reverses the action of SSRIs, which slow serotonin’s return to the presynaptic neuron. Serotonin instead remains in the cleft and repeatedly activates post-synaptic receptors."},{"text":"

Leaves the synapse through the bloodstream.
Activates fewer post-synaptic receptors.

","correct":false,"explanation":"SSRIs do not divert serotonin into the bloodstream or reduce receptor stimulation. By blocking reuptake, they keep serotonin in the synaptic cleft for longer."}]},{"id":"7ee654e7-654c-4e16-814a-d907295953f7","cardType":"basic","points":1,"front":"What did Cipriani et al. (2018) find about antidepressants?","back":"All 21 antidepressants, including SSRIs, beat placebos.","mcqOptions":[{"text":"All 21 antidepressants, including SSRIs, beat placebos.","correct":true,"explanation":"Cipriani et al.’s large meta-analysis found that each of the 21 antidepressants studied was more effective than placebo for the acute treatment of adult depression."},{"text":"Only SSRIs, but not other antidepressants, beat placebos.","correct":false,"explanation":"The findings were not limited to SSRIs. Cipriani et al. found that all 21 antidepressants studied, including drugs from several classes, were more effective than placebos."},{"text":"None of the 21 antidepressants, including SSRIs, beat placebos.","correct":false,"explanation":"This confuses criticisms of antidepressant effect sizes with the study’s actual result. All 21 antidepressants performed better than placebos, although their effectiveness varied."},{"text":"Only older antidepressants, excluding SSRIs, beat placebos.","correct":false,"explanation":"The evidence did not favour only older drug classes or exclude SSRIs. All 21 antidepressants examined, including SSRIs, were more effective than placebos."}]},{"id":"48ab126d-b5cd-4365-a309-17c059bdf608","cardType":"basic","points":2,"front":"What does the treatment-etiology fallacy warn against with SSRIs?","back":"Treatment success does not prove low serotonin caused depression.","mcqOptions":[{"text":"Treatment success does not prove low serotonin caused depression.","correct":true,"explanation":"A treatment can relieve symptoms without correcting the disorder’s original cause. Therefore, SSRIs working does not establish that depression was caused by low serotonin."},{"text":"Treatment success proves low serotonin caused depression.","correct":false,"explanation":"This is precisely the treatment-etiology fallacy: assuming a treatment’s mechanism reveals the disorder’s cause. Successful SSRI treatment does not prove that low serotonin caused depression."},{"text":"Treatment failure proves serotonin is unrelated to depression.","correct":false,"explanation":"A drug’s failure for one patient cannot establish that serotonin has no role in depression. The warning is that treatment success does not prove low serotonin caused depression."},{"text":"Treatment success proves high serotonin caused depression.","correct":false,"explanation":"SSRIs increase serotonin availability, but symptom improvement does not prove either a high-serotonin or low-serotonin cause. Treatment response cannot by itself establish etiology."}]},{"id":"949ba3a1-f4c2-4cf6-8a65-27a9c5180c58","cardType":"basic","points":1,"front":"Which problem can occur if SSRIs are stopped abruptly?","back":"Discontinuation syndrome.","mcqOptions":[{"text":"Discontinuation syndrome.","correct":true,"explanation":"Abruptly stopping SSRIs can produce discontinuation symptoms such as dizziness, nausea, anxiety and flu-like sensations because the nervous system has adapted to the medication."},{"text":"Serotonin syndrome.","correct":false,"explanation":"Serotonin syndrome is associated with dangerously excessive serotonergic activity, often from combining medications. Abrupt SSRI withdrawal instead risks discontinuation syndrome."},{"text":"Tardive dyskinesia.","correct":false,"explanation":"Tardive dyskinesia involves involuntary movements and is mainly linked to long-term antipsychotic use. Abruptly stopping SSRIs can instead cause discontinuation syndrome."},{"text":"Neuroleptic malignant syndrome.","correct":false,"explanation":"Neuroleptic malignant syndrome is a rare reaction usually associated with antipsychotic medication, not SSRI withdrawal. Sudden SSRI cessation can cause discontinuation syndrome."}]},{"id":"a2bf69aa-a49d-40c7-907a-6cdb2a058cb6","cardType":"basic","points":2,"front":"In Beck’s CBT, what does Patient as Scientist involve?","back":"Gather objective evidence to test negative beliefs.","mcqOptions":[{"text":"Gather objective evidence to test negative beliefs.","correct":true,"explanation":"Patient as Scientist treats beliefs as hypotheses rather than facts. The patient gathers real-world, objective evidence to evaluate whether negative beliefs are accurate."},{"text":"Gather subjective impressions to confirm negative beliefs.","correct":false,"explanation":"Relying on impressions and seeking confirmation would reinforce cognitive bias. Patient as Scientist instead gathers objective evidence to test whether negative beliefs are valid."},{"text":"Accept negative beliefs without testing their accuracy.","correct":false,"explanation":"Beck’s approach does not ask patients to accept negative beliefs uncritically. Patient as Scientist involves gathering objective evidence and testing those beliefs against reality."},{"text":"Replace all negative thoughts with positive beliefs.","correct":false,"explanation":"CBT aims for realistic, evidence-based thinking rather than forced positivity. Patient as Scientist gathers objective evidence to test the accuracy of specific negative beliefs."}]},{"id":"d3538025-05a2-4eb7-a079-02912e2a13b3","cardType":"cloze","points":null,"front":"In depression CBT, [ ] schedules pleasant activities to disrupt avoidance.","back":"In depression CBT, behavioural activation schedules pleasant activities to disrupt avoidance.","mcqOptions":[{"text":"behavioural activation","correct":true,"explanation":"Behavioural activation schedules rewarding or pleasant activities, interrupting the cycle in which low mood causes avoidance and reduced activity, which then deepens depression."},{"text":"cognitive restructuring","correct":false,"explanation":"Cognitive restructuring identifies and challenges distorted thoughts rather than primarily scheduling activities. Behavioural activation is the technique that uses planned pleasant activities to disrupt avoidance."},{"text":"systematic desensitisation","correct":false,"explanation":"Systematic desensitisation treats phobias by pairing gradual exposure with relaxation. Behavioural activation instead schedules pleasant activities to reduce avoidance in depression."},{"text":"psychoeducation","correct":false,"explanation":"Psychoeducation provides information about a disorder and its treatment, but it is not the activity-scheduling technique. Behavioural activation plans pleasant activities to disrupt avoidance."}]},{"id":"126b5a0d-28e2-4792-9e53-2f207c6212a5","cardType":"basic","points":2,"front":"Why can CBT reduce relapse compared with drugs alone?","back":"Patients learn lifelong strategies to intercept negative thoughts.","mcqOptions":[{"text":"Patients learn lifelong strategies to intercept negative thoughts.","correct":true,"explanation":"CBT teaches transferable skills for identifying and challenging negative thinking. Patients can continue applying these strategies after formal therapy ends, helping prevent future episodes."},{"text":"Patients receive permanent medication effects after therapy ends.","correct":false,"explanation":"CBT does not produce permanent medication effects, and drug benefits may diminish after treatment stops. Its relapse advantage comes from lifelong strategies for intercepting negative thoughts."},{"text":"Patients learn to suppress all negative thoughts permanently.","correct":false,"explanation":"CBT does not eliminate or permanently suppress every negative thought. It teaches lifelong strategies for recognising, evaluating and intercepting unhelpful patterns when they occur."},{"text":"Patients avoid all stressful situations after therapy ends.","correct":false,"explanation":"Avoidance can maintain psychological difficulties and is not CBT’s long-term goal. CBT reduces relapse by teaching lifelong strategies to identify and intercept negative thoughts."}]},{"id":"4dbe9651-b1de-4ad4-af8b-8a8985a0fad7","cardType":"basic","points":2,"front":"Why is CBT less accessible than drug therapy?","back":"It needs one-to-one trained therapy over several months.","mcqOptions":[{"text":"It needs one-to-one trained therapy over several months.","correct":true,"explanation":"CBT commonly requires repeated individual sessions with a trained therapist. Limited therapist availability, waiting lists and the lengthy commitment make it less accessible than prescribed medication."},{"text":"It needs daily medical supervision over several months.","correct":false,"explanation":"CBT does not normally require daily medical supervision. Its accessibility problem is the need for repeated one-to-one sessions with a trained therapist over several months."},{"text":"It needs expensive laboratory testing before every session.","correct":false,"explanation":"Laboratory testing is not a standard requirement for CBT. The main resource barrier is sustained one-to-one treatment with a trained therapist over several months."},{"text":"It needs continuous hospital admission throughout the treatment.","correct":false,"explanation":"Most CBT is delivered through outpatient sessions rather than continuous hospital admission. It is less accessible because trained one-to-one therapy is required over several months."}]},{"id":"31d3690b-d6b1-4f5b-a5bd-b6fc47328f59","cardType":"basic","points":2,"front":"What ethical concern can CBT create by focusing on thoughts?","back":"It may imply patient responsibility and ignore social stressors.","mcqOptions":[{"text":"It may imply patient responsibility and ignore social stressors.","correct":true,"explanation":"Emphasising faulty thoughts can suggest that patients are responsible for their disorder or recovery, while overlooking poverty, discrimination, relationships and other social causes of distress."},{"text":"It may imply therapist responsibility and ignore biological vulnerabilities.","correct":false,"explanation":"CBT’s focus on patients’ cognitions does not primarily place responsibility on the therapist. The ethical concern is that it may blame patients while overlooking social stressors."},{"text":"It may imply family responsibility and ignore unconscious conflicts.","correct":false,"explanation":"Focusing on thoughts does not specifically blame the patient’s family or neglect unconscious conflict. The concern is implied patient responsibility and insufficient attention to social stressors."},{"text":"It may imply institutional responsibility and ignore behavioural symptoms.","correct":false,"explanation":"CBT does not typically attribute responsibility to treatment institutions, and it often addresses behaviour directly. Its cognitive focus may instead imply patient responsibility and neglect social stressors."}]},{"id":"34f01b5c-e583-4a84-a644-a0667e1d1811","cardType":"basic","points":1,"front":"For a difference between independent groups using ordinal BDI scores, which test is appropriate?","back":"Mann-Whitney U test.","mcqOptions":[{"text":"Mann-Whitney U test.","correct":true,"explanation":"The Mann-Whitney U test assesses a difference between two independent groups when scores are ordinal, making it appropriate for comparing BDI scores in this design."},{"text":"Wilcoxon signed-rank test.","correct":false,"explanation":"The Wilcoxon signed-rank test is used for related or repeated-measures data. Independent groups with ordinal BDI scores require the Mann-Whitney U test."},{"text":"Spearman’s rho test.","correct":false,"explanation":"Spearman’s rho tests for a correlation between two co-variables rather than a difference between groups. The correct test for this independent-groups comparison is Mann-Whitney U."},{"text":"Independent t-test.","correct":false,"explanation":"An independent t-test is a parametric test requiring interval-level data and suitable distributional assumptions. Ordinal BDI scores from independent groups call for Mann-Whitney U instead."}]}]}],"examCountdown":{"examDate":"2027-05-18","paperLabel":"Paper 1"},"heading":"Treatments for the two disorders","title":"Treatments for the two disorders Flashcards","topbar":{"backHref":"/a-level/psychology/edexcel/flashcards"},"topicSidebar":"$L38"}]}],"topicId":"6cfbb4e8-8ff0-50ef-bff5-97c1129f114b","walled":"$L39"}],"$L3a","$L3b"]