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processes."},{"text":"psychological","correct":false,"explanation":"Psychological causes belong to explanations focused on thoughts, emotions or learning. The medical model instead assumes that mental disorders have biological causes."},{"text":"environmental","correct":false,"explanation":"Environmental influences are emphasised by behavioural and social explanations. The medical model primarily attributes mental disorders to biological causes within the body."},{"text":"spiritual","correct":false,"explanation":"Spiritual explanations attribute illness to supernatural forces rather than scientific bodily processes. The medical model assumes that mental disorders have biological causes."}]},{"id":"c1b73f56-094b-4d75-89eb-f587fcc6f115","cardType":"cloze","points":null,"front":"Neurotransmitters pass signals between nerve cells at a [ ].","back":"Neurotransmitters pass signals between nerve cells at a synapse.","mcqOptions":[{"text":"synapse","correct":true,"explanation":"A synapse is the junction between nerve cells. Neurotransmitters are released by one neuron and cross the synaptic gap to receptors on another."},{"text":"myelin sheath","correct":false,"explanation":"The myelin sheath insulates an axon and accelerates electrical transmission within a neuron. Neurotransmitters carry signals between neurons at a synapse."},{"text":"cell body","correct":false,"explanation":"The cell body contains the nucleus and maintains the neuron, but it is not the junction where neurotransmitters transmit signals. That junction is a synapse."},{"text":"node of Ranvier","correct":false,"explanation":"A node of Ranvier allows electrical impulses to travel rapidly along a myelinated axon. Chemical transmission between separate nerve cells occurs at a synapse."}]},{"id":"3841fced-a477-4094-a4f8-8e7e11b3cc8b","cardType":"basic","points":1,"front":"What does the dopamine hypothesis claim in schizophrenia?","back":"Unusual dopamine activity may contribute to symptoms.","mcqOptions":[{"text":"Unusual dopamine activity may contribute to symptoms.","correct":true,"explanation":"The dopamine hypothesis proposes that abnormal dopamine functioning contributes to schizophrenia, with different levels of activity in particular pathways associated with different symptoms."},{"text":"Unusual serotonin activity may contribute to symptoms.","correct":false,"explanation":"Serotonin may be relevant to some psychological disorders, but substituting it confuses different neurotransmitter explanations. The dopamine hypothesis specifically identifies unusual dopamine activity."},{"text":"Complete dopamine inactivity may contribute to symptoms.","correct":false,"explanation":"The hypothesis does not propose a total absence of dopamine. It links schizophrenia symptoms to unusually high or low dopamine activity in different neural pathways."},{"text":"Unusual GABA activity may contribute to symptoms.","correct":false,"explanation":"GABA is an inhibitory neurotransmitter, but it is not the focus of the dopamine hypothesis. The hypothesis claims unusual dopamine activity may contribute to schizophrenia symptoms."}]},{"id":"d5e08eb4-d85c-4bfd-8bac-f5b5ad9a4a55","cardType":"basic","points":1,"front":"Too much dopamine activity in some pathways is linked with which schizophrenia symptoms?","back":"Positive symptoms, such as hallucinations and delusions.","mcqOptions":[{"text":"Positive symptoms, such as hallucinations and delusions.","correct":true,"explanation":"Excessive dopamine activity, particularly in the mesolimbic pathway, is associated with positive symptoms that add experiences to normal functioning, including hallucinations and delusions."},{"text":"Negative symptoms, such as avolition and social withdrawal.","correct":false,"explanation":"Negative symptoms involve losses of normal functioning and are more closely associated with reduced dopamine activity in certain pathways. Excess dopamine is linked with positive symptoms."},{"text":"Cognitive symptoms, such as poor attention and working memory.","correct":false,"explanation":"Cognitive difficulties can occur in schizophrenia, but excessive dopamine activity is classically linked with positive symptoms, particularly hallucinations and delusions."},{"text":"Affective symptoms, such as depression and anxiety.","correct":false,"explanation":"Depression and anxiety are affective difficulties rather than the symptoms classically associated with excessive dopamine activity. Increased activity is linked with positive symptoms."}]},{"id":"a5f09d83-3e7f-4f54-b1cf-745e8b749155","cardType":"basic","points":1,"front":"Lower dopamine activity in other pathways is linked with which schizophrenia symptoms?","back":"Negative symptoms, such as reduced motivation.","mcqOptions":[{"text":"Negative symptoms, such as reduced motivation.","correct":true,"explanation":"Reduced dopamine activity, particularly in pathways involving the prefrontal cortex, is associated with losses of normal functioning such as reduced motivation and emotional expression."},{"text":"Positive symptoms, such as auditory hallucinations.","correct":false,"explanation":"Positive symptoms such as hallucinations are generally associated with excessive dopamine activity in particular pathways. Lower activity elsewhere is linked with negative symptoms."},{"text":"Cognitive symptoms, such as impaired working memory.","correct":false,"explanation":"Cognitive difficulties may accompany schizophrenia, but the dopamine account specifically links lower activity in certain pathways with negative symptoms such as reduced motivation."},{"text":"Affective symptoms, such as persistent low mood.","correct":false,"explanation":"Mood symptoms can coexist with schizophrenia, but they are not the category classically linked to reduced dopamine in this account. The expected category is negative symptoms."}]},{"id":"2f3d045a-71ba-42c1-996e-0e40734ca74f","cardType":"cloze","points":null,"front":"Serious mental disorders are often [ ], meaning many genes make small contributions.","back":"Serious mental disorders are often polygenic, meaning many genes make small contributions.","mcqOptions":[{"text":"polygenic","correct":true,"explanation":"Polygenic disorders involve the combined influence of many genes, with each genetic variant usually making only a small contribution to overall vulnerability."},{"text":"monogenic","correct":false,"explanation":"Monogenic means caused primarily by variation in one gene, which contradicts the involvement of many genes. Serious mental disorders are generally described as polygenic."},{"text":"oligogenic","correct":false,"explanation":"Oligogenic conditions involve a small number of influential genes, not many genes each making small contributions. The description given is polygenic."},{"text":"pleiotropic","correct":false,"explanation":"Pleiotropy occurs when one gene influences multiple characteristics. Many genes each contributing a small amount instead describes a polygenic disorder."}]},{"id":"0e7b193b-8f12-4c76-b31b-6eaa46e86b36","cardType":"basic","points":1,"front":"What does a child inherit in the genetic explanation of mental illness?","back":"A vulnerability, not a guaranteed disorder.","mcqOptions":[{"text":"A vulnerability, not a guaranteed disorder.","correct":true,"explanation":"Genes can create a predisposition that raises the probability of developing a mental disorder. Whether it develops also depends on environmental experiences and other factors."},{"text":"A single faulty gene, which inevitably causes illness.","correct":false,"explanation":"Complex mental disorders are not usually inherited as inevitable outcomes from one faulty gene. A child inherits genetic vulnerability, whose expression depends partly on other factors."},{"text":"A diagnosis, regardless of environmental experiences.","correct":false,"explanation":"A diagnosis is assigned through clinical assessment rather than inherited directly. What can be inherited is a vulnerability that increases the likelihood of developing a disorder."},{"text":"A specific symptom, not a general predisposition.","correct":false,"explanation":"Individual symptoms are not directly inherited as fixed outcomes. Genetic factors instead confer a broader vulnerability whose effects depend partly on environmental conditions."}]},{"id":"f007533e-b50f-4e61-936c-e4938c82a46e","cardType":"basic","points":1,"front":"In diathesis-stress, what can environmental stress do?","back":"Trigger a disorder in someone with vulnerability.","mcqOptions":[{"text":"Trigger a disorder in someone with vulnerability.","correct":true,"explanation":"Diathesis-stress proposes that environmental stress can activate an underlying biological or psychological vulnerability, leading to a disorder that might otherwise remain undeveloped."},{"text":"Cause a disorder equally in everyone exposed to stress.","correct":false,"explanation":"Diathesis-stress does not suggest everyone responds identically to stress. Stress triggers a disorder particularly when an individual already has an underlying vulnerability."},{"text":"Remove a genetic vulnerability before disorder develops.","correct":false,"explanation":"Environmental stress does not eliminate an inherited or pre-existing vulnerability. In the diathesis-stress model, it can trigger the development of a disorder."},{"text":"Prevent a disorder in someone with vulnerability.","correct":false,"explanation":"Stress is treated as a potential precipitating factor rather than protection from illness. It may trigger a disorder when combined with an existing vulnerability."}]},{"id":"8f373d08-7d49-4abd-9a50-1bf4e9911ea2","cardType":"basic","points":1,"front":"Why is the temporal lobe relevant to auditory hallucinations?","back":"It is involved in hearing and language.","mcqOptions":[{"text":"It is involved in hearing and language.","correct":true,"explanation":"The temporal lobe processes auditory information and supports language comprehension, so abnormal activity in this region could contribute to hearing voices that are not externally present."},{"text":"It is involved in vision and colour processing.","correct":false,"explanation":"Vision and colour processing are primarily functions of the occipital lobe. The temporal lobe is relevant because it processes hearing and language, which are central to auditory hallucinations."},{"text":"It is involved in balance and motor coordination.","correct":false,"explanation":"Balance and motor coordination are mainly associated with the cerebellum. The temporal lobe is relevant to auditory hallucinations because of its role in hearing and language."},{"text":"It is involved in touch and spatial awareness.","correct":false,"explanation":"Touch and spatial awareness are mainly associated with the parietal lobe. The temporal lobe is implicated because its hearing and language functions relate directly to experiencing voices."}]},{"id":"c9c166ba-c4ea-4605-b60a-18e47a5eb428","cardType":"basic","points":2,"front":"Why be cautious when interpreting brain abnormalities in schizophrenia?","back":"They may be a cause, consequence, or association.","mcqOptions":[{"text":"They may be a cause, consequence, or association.","correct":true,"explanation":"Observed brain differences do not establish direction of causality. They could produce schizophrenia, develop because of the disorder or its treatment, or merely be correlated with it."},{"text":"They must be a cause, symptom, or diagnosis.","correct":false,"explanation":"This assumes that abnormalities necessarily cause schizophrenia and confuses biological findings with symptoms or diagnoses. They may instead be a cause, consequence, or non-causal association."},{"text":"They may be a treatment, cure, or prevention.","correct":false,"explanation":"Brain abnormalities are biological observations, not interventions that treat, cure, or prevent schizophrenia. Caution is needed because they may be a cause, consequence, or association."},{"text":"They always show a cause, mechanism, or certainty.","correct":false,"explanation":"Finding an abnormality does not automatically reveal a causal mechanism or provide certainty. The difference may be a cause, a consequence of schizophrenia, or simply an association."}]},{"id":"494dcece-804b-4e35-a059-48020d683923","cardType":"basic","points":1,"front":"What type of study was Gottesman et al. (2010)?","back":"A population-based register study.","mcqOptions":[{"text":"A population-based register study.","correct":true,"explanation":"Gottesman et al. analysed population register data linking parental psychiatric diagnoses with schizophrenia outcomes in offspring, making the research a population-based register study."},{"text":"A laboratory-based experimental study.","correct":false,"explanation":"The researchers did not manipulate an independent variable under controlled laboratory conditions. They examined existing population records, so this was a population-based register study."},{"text":"A longitudinal clinical case study.","correct":false,"explanation":"A case study investigates one person or a very small group in depth. Gottesman et al. used large-scale population records, making it a population-based register study."},{"text":"A self-report questionnaire study.","correct":false,"explanation":"The data did not come primarily from participants reporting their own experiences in questionnaires. The researchers used official population registers to conduct a population-based register study."}]},{"id":"2eff050b-5e2b-4ae7-8eff-8ae83c6b2ed9","cardType":"basic","points":2,"front":"What schizophrenia risk did Gottesman et al. report for offspring with two schizophrenic parents vs the general population?","back":"About 27% vs about 1%.","mcqOptions":[{"text":"About 27% vs about 1%.","correct":true,"explanation":"Gottesman et al. found that approximately 27% of offspring with two schizophrenic parents developed schizophrenia, compared with roughly 1% in the general population."},{"text":"About 46% vs about 1%.","correct":false,"explanation":"The 46% figure is associated with other frequently cited genetic-risk estimates and overstates this study’s result. Gottesman et al. reported about 27% compared with about 1%."},{"text":"About 13% vs about 1%.","correct":false,"explanation":"The 13% figure is closer to estimates for offspring with one affected parent, not two. With two schizophrenic parents, the reported risk was about 27% versus 1%."},{"text":"About 27% vs about 10%.","correct":false,"explanation":"This correctly recalls the elevated offspring figure but overestimates the general population baseline by a factor of ten. The comparison was about 27% versus about 1%."}]},{"id":"4fcf16df-578f-4a40-a88d-0e743bf2c280","cardType":"cloze","points":null,"front":"Gottesman et al. found risk was not [ ], even when both parents were affected.","back":"Gottesman et al. found risk was not 100%, even when both parents were affected.","mcqOptions":[{"text":"100%","correct":true,"explanation":"Even with two affected parents, only about 27% of offspring developed schizophrenia. The risk was therefore not 100%, showing that genes do not determine the disorder completely."},{"text":"50%","correct":false,"explanation":"This confuses inheritance of a simple genetic characteristic with schizophrenia risk. The point was that risk did not reach 100%, even when both biological parents were affected."},{"text":"27%","correct":false,"explanation":"Approximately 27% was the observed risk for offspring with two affected parents, so saying the risk was not 27% contradicts the finding. It was not 100%."},{"text":"1%","correct":false,"explanation":"About 1% was the approximate risk in the general population, not the upper certainty level being rejected. The finding showed that risk was not 100%."}]},{"id":"256384ca-dcd0-4e9c-9396-d5531ba112d0","cardType":"basic","points":2,"front":"How does Gottesman et al. support the genetic explanation?","back":"Risk was higher when biological parents had psychiatric diagnoses.","mcqOptions":[{"text":"Risk was higher when biological parents had psychiatric diagnoses.","correct":true,"explanation":"The increased risk among offspring whose biological parents had psychiatric diagnoses is consistent with inherited vulnerability, so the findings support a genetic contribution to schizophrenia."},{"text":"Risk was higher when adoptive parents had psychiatric diagnoses.","correct":false,"explanation":"Attributing increased risk specifically to adoptive parents would support an environmental explanation based on upbringing. The genetic explanation is supported by higher risk linked to biological parents’ diagnoses."},{"text":"Risk was higher when teachers reported behavioural difficulties.","correct":false,"explanation":"Teachers’ reports of behaviour would concern observable development rather than inherited risk. Gottesman et al. supported genetics by linking higher risk to psychiatric diagnoses in biological parents."},{"text":"Risk was higher when families had lower socioeconomic status.","correct":false,"explanation":"A link with lower socioeconomic status would primarily suggest an environmental or social explanation. The genetic account was supported because risk increased with biological parents’ psychiatric diagnoses."}]},{"id":"58adba02-2f11-4055-95cf-c6fbb3933263","cardType":"basic","points":2,"front":"Why is Gottesman et al.'s huge sample a strength?","back":"It improves reliability and statistical power.","mcqOptions":[{"text":"It improves reliability and statistical power.","correct":true,"explanation":"A huge sample makes findings less vulnerable to unusual individuals and increases the chance of detecting genuine differences, thereby improving reliability and statistical power."},{"text":"It guarantees validity and cause and effect.","correct":false,"explanation":"A large sample cannot guarantee valid measurements or establish causation, especially in correlational research. Its main benefits are greater reliability and increased statistical power."},{"text":"It removes confounding variables and researcher bias.","correct":false,"explanation":"Increasing sample size does not automatically control shared environments, other confounding variables, or researcher bias. It mainly improves the reliability of findings and statistical power."},{"text":"It increases experimental control and ecological validity.","correct":false,"explanation":"Sample size alone does not create experimental control or determine ecological validity. The huge sample is valuable because it improves reliability and provides greater statistical power."}]},{"id":"04aab2ba-b5aa-4642-9a9f-29b5183d9ccd","cardType":"basic","points":2,"front":"Why is Gottesman et al.'s correlational design a weakness?","back":"It cannot prove genes caused the disorder because families share environments.","mcqOptions":[{"text":"It cannot prove genes caused the disorder because families share environments.","correct":true,"explanation":"A correlation between biological relatedness and schizophrenia does not isolate genetic influence. Relatives also experience similar environments, so the study cannot establish that genes caused the disorder."},{"text":"It cannot prove diagnoses were reliable because families share environments.","correct":false,"explanation":"Shared family environments create a problem for separating genetic and environmental causes, not for establishing diagnostic reliability. The design cannot prove that genes caused schizophrenia."},{"text":"It cannot prove the sample was large because families share environments.","correct":false,"explanation":"Sample size is established directly from the population registers and is unrelated to shared environments. The correlational weakness is that shared environments prevent proof that genes caused schizophrenia."},{"text":"It cannot prove registers were official because families share environments.","correct":false,"explanation":"Whether registers are official depends on their source, not on family environments. The real limitation is that shared environments confound the relationship, preventing proof of genetic causation."}]},{"id":"704a9277-80e4-4f93-a798-02984283a514","cardType":"cloze","points":null,"front":"Assuming Danish findings apply everywhere risks [ ].","back":"Assuming Danish findings apply everywhere risks ethnocentrism.","mcqOptions":[{"text":"ethnocentrism","correct":true,"explanation":"Ethnocentrism occurs when findings from one culture are treated as universally applicable, using that culture as the standard while overlooking meaningful cultural differences."},{"text":"androcentrism","correct":false,"explanation":"Androcentrism involves treating male experience as the norm, rather than generalising across cultures. Applying Danish findings everywhere risks ethnocentrism because one culture is assumed to represent all cultures."},{"text":"biological reductionism","correct":false,"explanation":"Biological reductionism explains behaviour using basic biological processes, such as genes or neurotransmitters. Generalising Danish findings to other cultures instead risks ethnocentrism."},{"text":"environmental determinism","correct":false,"explanation":"Environmental determinism assumes that behaviour is controlled by external influences. The issue here is ethnocentrism because findings from one national culture are being treated as universal."}]},{"id":"cbce9b0e-4be2-43bd-b401-0ef717dd3ef9","cardType":"basic","points":1,"front":"What is the main biological treatment for schizophrenia?","back":"Antipsychotic medication.","mcqOptions":[{"text":"Antipsychotic medication.","correct":true,"explanation":"Antipsychotic medication is the principal biological treatment for schizophrenia, acting on neurotransmitter systems to reduce symptoms, particularly positive symptoms such as hallucinations and delusions."},{"text":"Cognitive behavioural therapy.","correct":false,"explanation":"Cognitive behavioural therapy can help patients challenge distressing interpretations, but it is a psychological treatment. The main biological treatment for schizophrenia is antipsychotic medication."},{"text":"Family therapy.","correct":false,"explanation":"Family therapy aims to improve communication and reduce expressed emotion within families, so it is psychosocial rather than biological. Antipsychotic medication is the main biological treatment."},{"text":"Token economy programmes.","correct":false,"explanation":"Token economies use operant conditioning to reinforce desirable behaviour, making them behavioural treatments. The principal biological treatment for schizophrenia is antipsychotic medication."}]},{"id":"1c0bad9c-a8ef-45d9-9325-4bad857a444d","cardType":"basic","points":2,"front":"How do typical antipsychotics reduce positive symptoms?","back":"They block D2 dopamine receptors, reducing dopamine activity.","mcqOptions":[{"text":"They block D2 dopamine receptors, reducing dopamine activity.","correct":true,"explanation":"Typical antipsychotics act mainly as D2 receptor antagonists. Blocking these dopamine receptors lowers dopamine activity in relevant pathways, helping to reduce positive symptoms."},{"text":"They stimulate D2 dopamine receptors, increasing dopamine activity.","correct":false,"explanation":"This reverses the actual mechanism: greater D2 stimulation would be expected to worsen positive symptoms. Typical antipsychotics block D2 dopamine receptors and reduce dopamine activity."},{"text":"They block serotonin receptors, reducing serotonin activity.","correct":false,"explanation":"Serotonin receptor action is more strongly associated with atypical antipsychotics. Typical antipsychotics primarily reduce positive symptoms by blocking D2 dopamine receptors."},{"text":"They stimulate serotonin receptors, increasing serotonin activity.","correct":false,"explanation":"This confuses typical antipsychotics with mechanisms involving serotonin. Typical drugs mainly work by blocking D2 dopamine receptors, thereby reducing dopamine activity linked to positive symptoms."}]},{"id":"34a561a9-b2ad-409c-99f1-fa63f519d225","cardType":"cloze","points":null,"front":"Atypical antipsychotics affect dopamine and often [ ] systems.","back":"Atypical antipsychotics affect dopamine and often serotonin systems.","mcqOptions":[{"text":"serotonin","correct":true,"explanation":"Atypical antipsychotics act on dopamine and serotonin systems, often combining D2 dopamine antagonism with effects at particular serotonin receptors."},{"text":"GABA","correct":false,"explanation":"GABA is the brain’s main inhibitory neurotransmitter, but it is not the second system emphasised in the standard account of atypical antipsychotics. The correct term is serotonin."},{"text":"glutamate","correct":false,"explanation":"Glutamate has been investigated in explanations of schizophrenia, but standard atypical antipsychotics are described as affecting dopamine and serotonin systems."},{"text":"acetylcholine","correct":false,"explanation":"Acetylcholine contributes to functions such as memory and movement, but it is not the main additional system targeted in this account. Atypical antipsychotics often affect serotonin."}]},{"id":"7e61419e-87aa-45ad-8d9e-9659aa5f8345","cardType":"basic","points":1,"front":"Why does clozapine require medical monitoring?","back":"It can seriously affect white blood cells.","mcqOptions":[{"text":"It can seriously affect white blood cells.","correct":true,"explanation":"Clozapine can cause agranulocytosis, a dangerous reduction in infection-fighting white blood cells. Regular blood tests are therefore required to monitor the patient’s white blood cell count."},{"text":"It can seriously affect red blood cells.","correct":false,"explanation":"This confuses agranulocytosis with anaemia, which concerns red blood cells. Clozapine monitoring primarily checks for a dangerous reduction in white blood cells."},{"text":"It can seriously affect blood platelets.","correct":false,"explanation":"Platelets are mainly involved in blood clotting, but the characteristic serious risk requiring clozapine monitoring is agranulocytosis, which affects white blood cells."},{"text":"It can seriously affect bone marrow cells.","correct":false,"explanation":"Although clozapine’s adverse effects involve blood-cell production in bone marrow, monitoring specifically detects dangerously reduced white blood cells. The required answer is therefore white blood cells."}]},{"id":"1b4dee40-588d-4eda-be88-9e6e94709ffd","cardType":"basic","points":2,"front":"Why is antipsychotic medication useful for many patients?","back":"It can reduce distressing symptoms and relapse risk.","mcqOptions":[{"text":"It can reduce distressing symptoms and relapse risk.","correct":true,"explanation":"Antipsychotics can make symptoms such as hallucinations and delusions less distressing, while continued treatment may lower the likelihood of symptoms returning after improvement."},{"text":"It can improve memory function and social skills.","correct":false,"explanation":"Improved cognition and social ability are not the main established benefits, and some drugs may impair cognition. Antipsychotics are useful because they reduce distressing symptoms and relapse risk."},{"text":"It can eliminate underlying causes and all future symptoms.","correct":false,"explanation":"Medication manages symptoms rather than eliminating every underlying cause or guaranteeing a permanent cure. Its value lies in reducing distressing symptoms and lowering relapse risk."},{"text":"It can prevent all side effects and treatment resistance.","correct":false,"explanation":"Antipsychotics can themselves produce side effects, and some patients remain treatment-resistant. Their usefulness comes from reducing distressing symptoms and the risk of relapse."}]},{"id":"531de45d-1932-4189-8480-cc106f930646","cardType":"basic","points":2,"front":"Why can biological treatment of schizophrenia be criticised as reductionist?","back":"It may ignore trauma, family, social stress, poverty and culture.","mcqOptions":[{"text":"It may ignore trauma, family, social stress, poverty and culture.","correct":true,"explanation":"A purely biological approach reduces schizophrenia to factors such as genes and neurotransmitters, potentially neglecting important psychological, family, socioeconomic and cultural influences."},{"text":"It may ignore dopamine, genes, brain structure, neural activity and biochemistry.","correct":false,"explanation":"These are precisely the biological factors emphasised by the medical model, not factors it typically ignores. Reductionism is criticised for neglecting trauma, family and wider social influences."},{"text":"It may ignore diagnosis, classification, reliability, validity and symptom measurement.","correct":false,"explanation":"These concern how schizophrenia is identified and assessed rather than why biological treatment is reductionist. The criticism is that it overlooks trauma, family, social stress, poverty and culture."},{"text":"It may ignore dosage, absorption, metabolism, receptor binding and drug half-life.","correct":false,"explanation":"These are pharmacological details that biological treatment can readily consider. The reductionism criticism instead focuses on neglecting broader psychological, family, social, economic and cultural factors."}]},{"id":"41a95664-1052-4593-944c-ecbb96a4f17b","cardType":"basic","points":2,"front":"How can antipsychotic side effects reduce effectiveness?","back":"Unpleasant side effects can cause non-adherence.","mcqOptions":[{"text":"Unpleasant side effects can cause non-adherence.","correct":true,"explanation":"Patients may stop taking medication or take it inconsistently when side effects are unpleasant. This non-adherence reduces symptom control and increases the likelihood of relapse."},{"text":"Unpleasant side effects can cause treatment resistance.","correct":false,"explanation":"Treatment resistance means symptoms do not respond adequately despite suitable treatment; it is not simply caused by side effects. Side effects reduce effectiveness by encouraging non-adherence."},{"text":"Unpleasant side effects can cause faster drug metabolism.","correct":false,"explanation":"Drug metabolism is primarily determined by physiological and genetic factors, not by how unpleasant side effects feel. Side effects reduce effectiveness when they lead to non-adherence."},{"text":"Unpleasant side effects can cause diagnostic unreliability.","correct":false,"explanation":"Diagnostic unreliability concerns clinicians reaching inconsistent diagnoses, rather than patients’ responses to medication. Unpleasant side effects reduce treatment effectiveness by causing non-adherence."}]}]}],"examCountdown":{"examDate":"2027-05-10","paperLabel":"Paper 1"},"heading":"The medical model","title":"The medical model Flashcards","topbar":{"backHref":"/as-level/psychology/ocr/flashcards"},"topicSidebar":"$L38"}]}],"topicId":"560db943-a71b-5e93-8d8b-33aafa9a8b0c","walled":"$L39"}],"$L3a","$L3b"]