Biomedical treatments of psychological disorders Flashcards
(111 cards)
1
Q
What is the main assumption of the biological approach to mental illnesses?
A
assumes that all behavior has biological correlates, such as changes in brain activity and/or structure
2
Q
What is psychopathology?
A
study of abnormal states of mind
3
Q
What is descriptive psychopathology?
A
objective description of abnormal states, focusing on conscious experiences and observable behavior without preconceived ideas or theories
4
Q
What is the goal of experimental psychopathology?
A
aims to explain and describe abnormal mental phenomena, focusing on causes of symptoms within the context of syndromes where symptoms occur (Cowen, Harrison, Burns, 2012)
5
Q
What are psychological disorders according to the biomedical model?
A
illnesses or diseases that affect the nervous system
6
Q
How does the biomedical model explain abnormal behavior, thinking, and emotion?
A
views abnormal behavior, thinking, and emotion as results of biological dysfunctions in the brain
7
Q
What is the role of biochemistry in abnormal behavior?
A
imbalance of neurotransmitters or hormones can cause brain regions to malfunction, affecting behavior
8
Q
How does structural damage or abnormality affect mental health?
A
Brain damage or improper formation can alter thinking, emotion, and behavior
9
Q
What factors affect nervous system functioning?
A
- Genetics: inherited developmental abnormality
- Toxicity: chemical poisoning e.g drugs & environmental toxins
- Infection/disease: causing chemical or structural damage to the brain
- Stress: causing abnormal hormonal effects in the long term
10
Q
What is the p-factor in psychopathology?
A
general factor for psychopathology, similar to the g-factor for intelligence
11
Q
What is a key issue with the p-factor’s model fit?
A
p-factor mistakenly equates a good model fit with validity, which may not be accurate
12
Q
How does the p-factor support weak theories?
A
through underspecified construct validation efforts
13
Q
What replication issues are associated with the p-factor?
A
produces poorly replicated general factors of psychopathology
14
Q
What assumption does the p-factor violate?
A
violates assumptions of latent variable models
15
Q
How is the p-factor sometimes mistakenly treated?
A
as a latent, causal entity despite limited evidence
16
Q
What does family history suggest about depression and anxiety?
A
provides strong evidence for depression and anxiety risk
17
Q
What is ex vivo gene therapy?
A
removing target cells from the patient, modifying them to correct the disease phenotype, then returning them to the body
18
Q
How does in vitro gene therapy work?
A
corrected cells are prepared outside the body and then re-infused into the patient
19
Q
What is in situ gene therapy?
A
involves administering a viral vector directly to a specific organ
20
Q
Why is gene therapy limited?
A
limited application in psychological disorders because there are no clear genes to target
21
Q
What is the diathesis-stress model?
A
explains a disorder as the result of an interaction between predisposition vulnerability (diathesis) and stress from life experiences
22
Q
Victorian Treatments for Mental Health
A
- Moral Treatment: Patients were encouraged to engage in calming activities to improve mental well-being.
- Restraints and Isolation
- Hydrotherapy: Immersion in warm or cold water, thought to have a calming effect on patients.
- Bloodletting and Purging: Based on the belief that mental illness stemmed from imbalances in bodily fluids.
- Institutionalization
- Sedatives and Early Drugs
23
Q
What is a core belief of the biomedical model regarding mental and physical diseases?
A
no meaningful distinction between mental diseases and physical diseases
24
Q
What are the main types of treatments in the biomedical model?
A
Psychosurgery, electroconvulsive therapy (ECT), and psychopharmacotherapy
25
What does psychosurgery involve in the context of contemporary mental health treatment?
Brain surgery to treat mental disorders
26
What is psychopharmacotherapy?
use of medication to manage or treat mental disorders
27
Which brain regions are targeted in modern psychosurgery?
pathways between the limbic system and the frontal cortex
28
What is the role of the limbic system and frontal cortex in psychosurgery?
limbic system regulates emotions, while the frontal cortex is involved in thought processes
29
What was the leucotomy/frontal lobotomy, and when did it peak?
procedure developed by Egas Moniz that involved removing white matter fibres in the frontal lobe to treat mental illness, peaking between 1950-1950
30
Who performed frontal lobotomies and how?
Freeman performed about 3,600 lobotomies, often using an ice pick inserted through the eye socket
31
What were the side effects of frontal lobotomies?
Personality changes, epilepsy (10-35% of patients), and deaths due to bleeding
32
What is neurosurgery for mental disorders (NMP)?
modern variation of psychosurgery involving the destruction of small areas of the brain, with patient consent, used for severe cases of mental illness when other treatments fail
33
How does deep brain stimulation (DBS) differ from traditional psychosurgery?
involves inserting electrodes into the brain and a stimulator under the skin in the chest to modulate brain activity, rather than severing connections
34
What is Electroconvulsive Therapy (ECT)?
treatment where an electric current is passed between two scalp electrodes to induce a seizure in the brain
35
What preparations are made before ECT is administered?
Patients are given short-acting barbiturates to induce unconsciousness and a nerve-blocking agent to prevent muscle contractions during the seizure
36
How many ECT treatments does a patient usually receive?
typically receives between 3 and 15 ECT treatments
37
When was Electroconvulsive Therapy first used?
since the 1930s
38
What are some short-term side effects of ECT?
Side effects include retrograde and anterograde amnesia (both short and long-term), depressive symptoms, headaches, sore muscles, and feelings of fear
39
What does "chemical imbalance" refer to?
refers to variations in neurotransmitters in the brain that are responsible for transmitting messages
40
What are the phases of clinical trials?
- Safety: Is the medication safe?
- Efficacy: Is the medication effective in treating the targeted condition?
- Confirmation: How does the treatment compare to standard treatment?
- Follow-up: After approval, how does the medication work for other patients?
41
What is the structure of a randomised controlled trial (RCT)?
- Define the population
- Select a sample (exclusions based on age and other conditions)
- Randomly divide the sample into groups: one for active treatment, one for placebo, and possibly one for a no-treatment/waiting list control group.
- Measure outcomes and compare different groups
42
What does "blind" and "double-blind" mean in clinical trials?
- Blind: The patient does not know which group they are in, but the doctor does
- Double-blind: Neither the patient nor the doctor knows which group the patient is in
43
What did Paul (1966) find about the placebo effect in medical treatments?
placebo effect is found in all medical treatments, with variations from 15% to 72%. It can induce changes in brain activity, neurotransmitters, and hormones, not just positive thinking
44
In which areas is the placebo effect strongest?
pain, depression, anxiety, insomnia, and nausea studies, with some studies estimating effects as high as 90%
45
What did Ashar, Chang, & Wager (2017) suggest about the placebo effect in psychological treatments?
suggested that many psychological treatments may have beneficial effects because the client expects them to work, rather than because the treatment is effectively addressing the underlying psychopathology
46
What is the nocebo effect?
when a treatment is perceived as harmful or inactive, potentially exacerbating symptoms and outcomes. It is more likely to cause side effects than a placebo
47
What is spontaneous remission?
recovery from a mental health condition without any treatment
48
What percentage of untreated cases of depression spontaneously remit over time?
23% of untreated cases of depression will spontaneously remit within 3 months, 32% within 6 months, and 53% within 12 months (Whiteford, 2013)
49
What are some potential explanations for spontaneous remission?
Potential explanations include regression to the mean, resilience, neuroplasticity, and natural recovery
50
Why can't all treatment success be attributed to drugs alone?
Individuals in treatment groups may also experience spontaneous remission (p & sr), meaning not all success can be attributed solely to the drug
51
Why might some clinical trial results be hidden or delayed?
Some companies may share only positive results and hide or delay negative findings to maintain the perceived efficacy of their products
52
What is a criticism of Big Pharma regarding mental illness?
accused of creating and exploiting a manufactured epidemic of mental illness by over-diagnosing and overprescribing drugs that are not always necessary, effective, or safe
53
How does Big Pharma's approach promote a medical model of mental illness?
promotes a medical model that may overlook or undermine other important factors, such as social, psychosocial, psychological, environmental, and cultural influences
54
What is the main driving force behind pharmaceutical companies' actions?
driven by profit rather than reducing suffering, which raises concerns about the prioritization of business interests over patient well-being
55
What is a growing interest in the field of psychiatry, and why is it controversial?
There is growing interest in using psychedelics like psilocybin, MDMA, and ketamine, but their legal status and potential harms make their use controversial
56
How might the pharmaceutical industry approach psychedelics like psilocybin?
aim to develop engineered or synthetic versions of psychedelics, even if they may pose more harm than natural ones
57
What are some ethical issues with pre-human animal trials in pharmaceutical research?
Many pre-human trials are conducted on animals, but rats and other animals do not suffer from depression, raising questions about the relevance and ethics of such studies
58
What is a limitation of pharmaceutical treatments for mental illness?
may reduce biological risk factors but do not address all of them, and they do not improve protective factors or teach coping and problem-solving skills
59
What are the challenges associated with discontinuing psychiatric medication?
high relapse rate and the potential for aversive "discontinuation syndrome" when clients stop taking drugs, complicating the recovery process
60
What do Hofmann and Hayes suggest regarding clinic-based research?
Hofmann and Hayes suggest that clinics should be used as a prime source of data, as it would generate knowledge from a diverse group of clients
61
What does using clinic-based research encourage in therapeutic approaches?
encourages a process-based approach that focuses on mediators and moderators of therapeutic outcomes
62
What is the effect of clinic-based research on broad-level therapies?
leads to the decline of broad-level therapies that rely on set techniques, instead promoting more individualized therapeutic processes
63
What are the most common anti-anxiety drugs?
benzodiazepines, such as clonazepam and diazepam
64
What are the effects of benzodiazepines?
fast-acting and powerful, providing immediate relief from acute anxiety attacks but have significant side effects, including drowsiness, confusion, memory loss, and coordination problems
65
What types of drugs are used for long-term treatment of anxiety disorders?
For long-term anxiety disorders, antidepressants are used as they are slower-acting but long-lasting
66
What are the three classes of antidepressant drugs?
Tricyclics: Prevent reuptake of excitatory transmitters, but have severe side effects.
Monoamine oxidase (MAO) inhibitors: Reduce the activity of MAO, increasing norepinephrine and serotonin activity.
Selective serotonin reuptake inhibitors (SSRIs): Increase serotonin activity by preventing its reuptake and have milder side effects
67
How do SSRIs compare to other antidepressants?
SSRIs are more effective at reducing depressive symptoms rapidly and have milder side effects compared to other antidepressants like tricyclics and MAO inhibitors.
68
How do antidepressants affect serotonin?
Antidepressants increase serotonin (5HT) availability in the brain, either by increasing release or blocking reuptake, but the exact effect on serotonin activity remains unclear
69
What is the pragmatic approach to serotonin in depression?
pragmatic approach suggests that while serotonin may not be the direct cause of depression, increasing its availability through antidepressants can alleviate symptoms, much like how paracetamol can relieve a headache without being the cause
70
How does tryptophan affect serotonin and depression?
Lowering dietary tryptophan can lead to depression relapse in patients already treated with SSRIs and may induce depression in healthy controls
71
How has the number of prescriptions for antidepressants in the UK changed in recent years?
The number of antidepressant prescriptions in the UK has increased steadily over the last decade, from 64.7 million in 2015/16 to 79.2 million in 2019/20
72
What is a notable trend in prescription rates for intellectual disabilities?
People with intellectual disabilities are often overprescribed psychotropic drugs, with the proportion receiving treatment far exceeding the proportion diagnosed with mental illness (Sheehan, 2015)
73
What are some alternative treatments that could be more beneficial than antidepressants for everyday suffering?
For everyday suffering, people might benefit more from preventative training, low-level counselling, or education instead of relying on antidepressants
74
What are some significant concerns regarding antidepressant medications?
Antidepressants are not benign treatments. Many are cardiotoxic, have dangerous side effects, and are often used in suicide attempts
75
What is the non-response rate for antidepressant medications in certain patient populations?
Some patient populations experience up to a 60% non-response rate to antidepressant medications
76
Why might antidepressants be ineffective for some individuals?
Medications target common symptoms, but these symptoms may not be shared by all individuals or may vary in severity, failing to address the individual's suffering and lived experience
77
What does the Power Threat Meaning Framework (PTMF) focus on instead of traditional psychiatric diagnosis?
focuses on understanding the role of power, threats, and meaning in people's lives, rather than relying on traditional psychiatric diagnoses
78
What are the three core components of the PTMF?
The three core components of PTMF are:
- Power - The influence of social, economic, and cultural power on individuals
- Threat - The types of threats that arise from the misuse of power, such as discrimination, abuse, and inequality
- Meaning - How individuals make sense of their experiences and the importance of personal narratives
79
What is a key claim of the Power Threat Meaning Framework (PTMF)?
the current approach to the causality of human distress will always be probabilistic, offering only average characteristics, not a precise understanding of the impacts
80
What are some criticisms of the Power Threat Meaning Framework (PTMF)?
- PTMF’s rejection of the medical model, failing to distinguish between physiological dysfunction and subjective experience
- It reduces complex mental health issues to simple cause-and-effect relationships involving power and threat
- Some mental health professionals question its practical applicability in clinical settings
- Lack of empirical evidence
81
What were the findings of the Lancet publication
All 21 antidepressants were found to be more likely to work than placebo, but effectiveness varied between different drugs and placebo
82
What were the key limitations of the Lancet publication?
- It only reported results after 8 weeks of treatment, leaving long-term results unaddressed.
- 78% of studies were funded by drug manufacturers.
- It did not allow conclusions about drug effectiveness versus talking therapies.
- It did not account for participant idiosyncrasies, such as how drugs work across different ages, sexes, and social-economic statuses.
- There could be a problem with the idea of an adequate placebo for antidepressants
83
What was the objective of the Lancet study comparing second-generation antidepressants (fluoxetine) to others and to placebo over 8 weeks?
to evaluate how effective fluoxetine is compared to other antidepressants and placebo, defined as a reduction in depression symptoms of >50% after 8 weeks
84
What does the Dopamine hypothesis suggest about psychotic symptoms?
suggests that increased dopamine levels contribute to the positive symptoms of schizophrenia, as supported by drug studies showing that amphetamines, which increase dopamine levels, produce similar symptoms (delusions & hallucinations) to schizophrenia
85
What are typical antipsychotics used for, and what are their side effects?
(e.g., chlorpromazine, haloperidol, trifluoperazine) are used to treat psychotic symptoms such as delusions and hallucinations, especially in schizophrenia and bipolar disorder. They temporarily occupy D2 dopamine receptors and then dissociate to allow normal dopamine transmission. They are associated with significant side effects, including tardive dyskinesia (5% of patients)
86
What are atypical antipsychotics, and how do they differ from typical ones?
(e.g., clozapine, olanzapine, risperidone, quetiapine) are used to treat both positive and negative symptoms of schizophrenia. They are more effective than typical antipsychotics in treating negative symptoms and have fewer side effects, including a lower risk of tardive dyskinesia. Studies show that atypical antipsychotics benefit 85% of schizophrenia patients, compared to 65% with typical drugs (Meltzer, 1999)
87
What do studies show about relapse rates in patients on antipsychotic medications versus placebo?
55% of patients on placebo experience relapse, compared to 19% for those who remain on the drug (Davis, 1980). However, Ross & Read (2004) argue that the 45% of placebo patients who benefitted indicate that many on the drug would have responded to the placebo. Emsley (2018) found relapse rates as high as 77% in the first year, and 90% in the second year
88
What are chemical lobotomies?
"chemical lobotomy" critiques antipsychotics due to their sedative effects, which can cause patients to appear emotionally blunted, unresponsive, and disconnected. While these drugs were not intended to function as a lobotomy, their sedative effects sometimes led to this comparison
89
What are the main characteristics of Borderline Personality Disorder (BPD)?
characterized by a pervasive pattern of instability in mood, self-image, and interpersonal relationships. Individuals often struggle with intense, unstable relationships, can be intolerant of being alone, and may exhibit manipulative behavior as an adaptive strategy to maintain attachment
90
How do individuals with Borderline Personality Disorder (BPD) typically express intense emotions?
express intense emotions through temper tantrums, physical aggression, or suicidal threats. Para-suicidal behavior (self-harm without the intent to die) is also common
91
What is the relationship between BPD and the biological aetiology, particularly neurotransmitter dysfunction?
Evidence suggests that BPD is linked to neurotransmitter dysfunction, particularly in serotonin and dopamine systems. A decreased functioning of serotonin systems is associated with impulsivity, which can manifest in emotional dysregulation and depressive episodes (Soloff, 2000).
92
What brain abnormalities are associated with Borderline Personality Disorder (BPD)?
frontal lobe, which is involved in impulse control, and the limbic system, particularly the amygdala. The amygdala, which plays a crucial role in emotional processing and regulation, shows increased activation in individuals with BPD (Herpetz, 2001), which may contribute to emotional instability.
93
What are the primary drug treatments for Borderline Personality Disorder (BPD)?
- Anti-psychotics (Neuroleptics): Block dopamine to reduce symptoms like impulsivity and aggression.
- Antidepressants: Tricyclics and MAOIs increase noradrenaline; SSRIs target serotonin deficiency.
- Mood Stabilizers: Used for mood regulation, especially in impulsivity and emotional dysregulation
94
What evidence supports the use of anti-psychotics in treating BPD?
Anti-psychotics improve symptoms like impulsivity, affective dysregulation, and cognitive disturbances.
However, the evidence is limited and not definitive for all symptom clusters
95
Are antidepressants effective in treating depressive symptoms in BPD?
SSRIs: Generally found to be unhelpful for treating BPD-related depressive symptoms.
Tricyclics & MAOIs: Increase noradrenaline, but effectiveness is less clear in BPD treatment
96
How do mood stabilizers benefit BPD treatment?
help regulate mood, especially in addressing impulsivity and emotional instability
97
Why might patients with BPD be prescribed a combination of drugs?
Due to comorbid conditions (e.g., depression, anxiety
98
What is lithium carbonate used to treat?
Used to treat bipolar disorder.
Effective in treating the mania phase and can also help regulate depressive symptoms
99
What are the risks of suddenly stopping lithium carbonate?
Sudden withdrawal can lead to various medical problems, including relapse of symptoms or other complications
100
What are the long-term side effects of lithium carbonate?
Long-term use can cause thyroid disorders, as well as mild cognitive and memory impairment
101
How were social and recreational drugs historically viewed in mental health treatment?
In the early 1900s, drugs like cocaine were seen as wonder drugs with mental health applications
102
What is common between recreational drugs and psychopharmaceuticals?
tend to induce mood and perception changes and impact mental states in significant ways.
103
What are the effects of Ketamine on mood and perception?
Produces detachment and a chilled, happy feeling.
Can cause nausea, depression, memory loss, and numbness, making users unable to feel pain
104
What is Ketamine’s legal status and medical uses?
It is a class B substance in the UK.
FDA-approved for general anesthesia and severe pain relief.
105
What is Psilocybin, and where is it found?
Psychedelic compound found in some species of mushrooms.
Classified as a class A drug in the UK.
106
What were the results of psilocybin treatment on depressive symptoms?
large and rapid reduction in depressive symptoms that lasted several weeks or months for most participants
107
What did brain imaging data suggest about the effects of psilocybin on the brain?
increased neural connectivity and plasticity, which may help explain its therapeutic effects
108
What were some limitations of the psilocybin studies?
included small sample sizes, lack of blinding or active control groups, participant heterogeneity, and potential biases or confounding factors
109
What is the primary goal of drugs in the disease-centered model?
aim to correct an abnormal brain state and target the underlying disease process
110
How does the drug-centered model view the role of drugs?
sees drugs as creating an abnormal brain state, with therapeutic effects coming from the drug-induced state’s impact on behavioral and emotional issues
111
What effect do drugs have on behavior and emotions in the drug-centered model?
Drugs induce an abnormal brain state that alters or replaces psychological and behavioral symptoms
