Lecture 6-Biomedical Model Flashcards

1
Q

What are used to explain phenomenas in science?

A

Models (paradigms)

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2
Q

What do models do?

A

Spell out assumptions, give order to the field and give structured framework for investigation

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3
Q

What do models influence?

A

What investigators observe, the questions they ask, the infromation they seek and how they interpret data

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4
Q

How do research findings interpreted?

A

In the context of existing scientific models

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5
Q

What perspective is the bio model of mental disorders?

A

Medical and bio perspectives

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6
Q

What are the assumptions of the bio model?

A

Mental disorders are biologically based brain diseases
The cause is structural and physical
Mental disorders reflect something wrong with the brain structure or function

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7
Q

What is the aim of research for the biological model?

A

To uncover the bio cause of mental disorder

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8
Q

What is the emphasis of the bio model?

A

On medical treatment

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9
Q

What does the bio model argue?

A

There is no distinction between mental and physical diseases

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10
Q

What is maladaptive behaviour considered to be?

A

A function of interaction between biological, psychological and social factors

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11
Q

What has the bio model caused an increase of?

A

Use of pharmalogical agents in mental illnesses

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12
Q

What do PET scans show in depression?

A

Reduced brain activity in depression

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13
Q

What are the biological causes of mental disorders?

A

Neurotransmitters and hormones
Genetics
Developmental abnormalities
Physical deprivation, neglect or stress
Toxic agents

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14
Q

What are the three neurotransmitter imbalances?

A

Altered production, altered reuptake and alternations in neurotransmitter receptors

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15
Q

What is altered production?

A

Altered production of neurotransmitter at synapses, over or under-stimulating the target neuron

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16
Q

What is altered reuptake?

A

Altered reuptake of neurotransmitters, increasing or decreasing concentration at synapses

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17
Q

What is alternations in neurotransmitter receptors?

A

Alterations in neurotransmitter
receptors, so that they are abnormally sensitive or insensitive

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18
Q

Who looked at hormones?

A

Carlson, 2007

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19
Q

What did Carlson, 2007, find?

A

Dopamine, norepinephrine, serotonin, glutamate and GABA has been studied in relation to psychpathology

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20
Q

What are the 2 types of psychotropic drugs?

A

Agonist and antagonist

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21
Q

What are agonist drugs?

A

Drugs that increase neurotransmitters binding to receptors

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22
Q

What are antagonist drugs?

A

Drugs that decrease neurotransmitters binding to receptors

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23
Q

What do psychotropic drug increase?

A

Synaptic transmission

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24
Q

What are the psychotropic drug mechanisms?

A

Increase or decreased synthesis, increase or decrease transmitter re-uptake and direct stimulation or inhibition of transmitter receptors

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25
Q

What does drug discovery allow?

A

Sheds light on mechanisms of disease or understanding disease mechanisms allows rational drug design

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26
Q

What does resperpine do?

A

Treat high blood pressure but then caused depression and depletes nerve cells of amine neurotransmitters

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27
Q

What does iproniazid do?

A

Was an anti-tuberculosis drug and caused euphorbia, increased appetite and improved sleep as it increased amine neurotransmitters

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28
Q

What is depression caused by?

A

Deficiency of amine neurotransmitters

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29
Q

How do anti-depressants work?

A

Correct amine brain levels

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30
Q

What do SSRIs do?

A

Block the re-uptake of serotonin such as sertraline

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31
Q

What are criticism of amine hypothesis?

A

There are inconsistent findings
Poor control of confounding variables
Used small sample sizes
An oversimplification
Based theory on disease causation

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32
Q

What is the amine hypothesis of schizophrenia?

A

Excess of dopamine causing delusions and hallucination

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33
Q

What is the amine hypothesis of OCD?

A

Symptoms due to dysfunctions of brain pathways regulated by serotonin

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34
Q

What are the problems of bio models of disease?

A

Simplistic and misleading

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35
Q

What are characteristics of bio disease models?

A

Complex and suppirted by extensive research evidence such as animal models, autopsy, fMRIs and genetics

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36
Q

What is the endocrine system?

A

System of glands that secrete hormones in the bloodstream

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37
Q

What are hormones?

A

Chemical messengers that control body functions

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38
Q

What is the main gland?

A

Pituitary

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39
Q

What is the pituitary controlled by?

A

Hypothalamus

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40
Q

What can over activity in stress states cause?

A

Chronic psychological stress for elevation of cortisol (leads to depression + anxiety)

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41
Q

What are the genetic vulnerabilities?

A

Chromosomal abnormalities and single gene defects

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42
Q

Who looked at genetic vulnerabilities?

A

Ploemin et al

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43
Q

What did Ploemin et al find?

A

There is evidence that disorders have genetic influence

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44
Q

What are chromosomal abnormalities?

A

Complete or partial duplications/deletions

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45
Q

What are single gene defect?

A

Abnormalities in particular genes or disease associated normal variants

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46
Q

What does polygenic mean?

A

Vulnerabilities to mental disorders

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47
Q

Who looked at polygeny?

A

Kendler, 2005

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48
Q

What did Kendler, 2005, find?

A

Disorders are influenced by multiple genes causing genetic vulnerability

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49
Q

What is epigenetics?

A

Genes being switched on and off

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50
Q

How are genes silenced?

A

Adding of molecular tags to parts of the DNA strand

51
Q

What is gene methylation influenced by?

A

Environment such as early life experiences

52
Q

What can adverse life experience lead to?

A

Epigenetic changes that influence a risk of disorders

53
Q

What is the gene-environment interaction?

A

Behaviour not being determined by genes you inherit but due to genetics and the environment

54
Q

Who looked at gene-environment interaction?

A

Culverhouse et al

55
Q

What did Culverhouse et al do?

A

Tested 30 datasets with 40000 people

56
Q

Who looked at the ways genotype can shape environment?

A

Jang et al

57
Q

What did Jang et al find?

A

The three ways that genotype can shape the environment:
Genotype can have a passive effect on environment
Genotype can cause certain reactions to environment
Genotype can play a more active role in shaping environment

58
Q

Who looked at genotype can have a passive effect on environment?

A

Rutter 2006

59
Q

What did Rutter, 2006, find?

A

Antisocial behaviour can create a risky environment so there is a higher chance of mental disorders

60
Q

Who looked at genotype can cause certain reactions to environment?

A

Lytton 1980

61
Q

What did Lytton find?

A

Happy babies drawing more positive responses from passive infants

62
Q

Who looked at genotype can play a more active role?

A

Plomin et al

63
Q

What did Plomin et al find?

A

Extraverted children seeking the company of others which can cause them to be sociable

64
Q

What are the methods for studying genetic influences?

A

Family history method, twin method and the adoption method

65
Q

What are the aims of bio model treatment?

A

Target underlying bio dysfunction

66
Q

Who looked at the goal of bio model treatment?

A

Moncrieff, 2008

67
Q

What is the goal of bio model treatment?

A

Discover precise therapeutic agents that target the disease process without causing harm

68
Q

What are the treatments for biomedical model treatment?

A

Pharmocological, brain stimulation or surgery

69
Q

Who found insulin shock therapy?

A

Manfred Sakel

70
Q

What is insulin shock therapy used for?

A

Schizophrenia in 40-50s to induce coma

71
Q

What are the risks of insulin shock therapy?

A

Obesity, seizures and brain damage

72
Q

Who found the prefrontal leukotomy?

A

Egaz Moniz

73
Q

Who found the frontal lobotomy?

A

Walter Freeman

74
Q

What does a frontal lobotomy do?

A

Reduce emotional distress and improved challenging behaviour. Caused flat, passive and unemotional behaviour

75
Q

Who found electroconvulsive therapy?

A

Ugo Cerlatti and Lucio Bini

76
Q

What is ECT?

A

Controlled induction of convulsive seizures under general anaesthesia

77
Q

What does ECT effect?

A

Numerous neurochemical systems

78
Q

What are the criticism of ECT?

A

High relapse rates

79
Q

What does deep brain stimulation do?

A

Stimulation of area 25 in the limbic lobe associated with mood improvement in severe depression

80
Q

What is deep brain stimulation used for?

A

Severe treatment resistant conditions

81
Q

Who looked at DBS?

A

Mayberg et al

82
Q

What did Mayberg et al find?

A

DBS can be effective

83
Q

What are the criticisms of DBS?

A

It is very expensive and carries risks

84
Q

What is TMS used for?

A

Treatment resistant depression and anxiety disorder

85
Q

What happens in TMS?

A

Electromagnetic coil delivers magnetic pulses to the brain and can be targeted to specific areas

86
Q

Who looked at TMS?

A

Slotema, Blom, Hoel and Sommer

87
Q

What did Slotema, Blom, Hoel and Sommer find?

A

Meta analysis where it was found TMS is effective for acute depression but not as good as ECT

88
Q

What are the forms of medical treatment for mental disorders?

A

Antidepressants, anxiolytics, anti-psychotics and mood stabilisers

89
Q

What are the side effects of antidepressant agents?

A

Nausea, nervousnessm insomnia and sexual dysfunction

90
Q

When is antidepressant agents recommended?

A

When there is no response to psychological treatment and depressive symptoms are severe

91
Q

When are anxiolytics used?

A

If guided self-help and
cognitive-behavioural therapy (CBT) fails

92
Q

What do benzodiazepines do?

A

Sedative and muscle-relaxing properties
Cause drowsiness and lethargy
Highly addictive, high relapse rates

93
Q

What are antipsychotic drugs used for?

A

To treat psychotic disorders and act by
blocking brain dopamine (and/or serotonin) receptors

94
Q

Who looked at antipsychotics with people with schizophrenia?

A

Sharif et al, 2007

95
Q

What did Sharif et al find?

A

Antipsychotics had positive results on people with schizophrenia

96
Q

What are the side effects of antipsychotics?

A

Weight gain, diabetes and reduced white blood cell count

97
Q

What is lithium used for?

A

Bipolar affective disorder

98
Q

What are the risk of lithium?

A

Mechanism uncertainty and risk of toxicity

99
Q

How effective is bipolar disorder?

A

70-80%

100
Q

Who looked at lithium on bipolar disorder?

A

Keck and McElroy, 2007

101
Q

What did Keck and McElroy find?

A

High rates of discontinuaton, 50% at 6 months

102
Q

What are the side effects of lithium?

A

Thirst, weight gain,
gastrointestinal difficulties, tremor, fatigue

103
Q

What are the advantages of the biomedical approach?

A

Suggests clear mechanism for most disorders
Effective in delivering insights into disorders with a clearer bio base
Drug treatment has revolutionised patient care and is more effective
Treatment is based on the scientific method

104
Q

What research evidence is used for the biomedical approach?

A

A randomised control trial with double blind studies
Meta analysis to use results from different trials

105
Q

What are the limitation of the biomedical approach?

A

Assumes universality (no room with its framework for social, psychological disorders)
Reductionism
Low causality
Claims mental disorders are brain disease cause by ntm genetic anomalities and defects in brain stricture but scientists have no identified a biological cause
Stigma from mental disorders

106
Q

What is diagnosis based on?

A

Classification system with specified symptoms

107
Q

What may the symptoms do to qualify for mental disorders?

A

Cause clinical distress and impairment in social, occuptational or important areas of function

108
Q

Who developed classification system for mental disorders?

A

Emil Kraepelin

109
Q

What did Emil Kraepelin emphasise?

A

The importance of brain pathology in mental
disorders (medical model)

110
Q

Has mental disorders increased or decreased in the DSM?

A

Increased

111
Q

What was the DSM I characteristics?

A

No diagnostic criteria
Grounded in psychodynamic formulations of mental disorders
Established by psychoanalysts
Disorders described with prototypes that are narrative descriptions of disorders

112
Q

What was the DSM II characteristics?

A

Psychoanalysis still dominated
Psychoneurotic problems redefined as
‘neurotic’ disturbances
No clear descriptions of ‘disorders’
All ‘symptoms’ defined as ‘symbolic’ of
unconscious processes

113
Q

What was the DSM III characteristics?

A

Relied to a much greater extent on empirical data
Included specific diagnostic criteria
Dropped allegiance to a particular theory of therapy or psychopathology
Introduced the multiaxial assessment that remained until the DSM IV-TR

114
Q

What was the DSM III-R
characteristics?

A

Renamed, added, and deleted categories
Pressure groups had an influence
Changes to diagnostic criteria
Increased reliability

115
Q

What was the DSM IV
characteristics?

A

The term ‘neurosis’ was dropped
Conservative approach
Inclusion of a clinical significance criterion to almost half of all the categories, which required that symptoms cause: “clinically significant distress or impairment in social, occupational, or
other important areas of functioning”

116
Q

What was the DSM V
characteristics?

A

Most substantial revision in the last 20 years
Clearly influenced by the (bio)medical model of mental disorders
The DSM-5 does not include all possible mental disorders
The cultural and social context must be considered
Making diagnoses requires clinical judgment, not just checking
off the symptoms in the criteria
Diagnoses are made on the basis of: Clinical interview., DSM-5 text descriptions and criteria, clinical judgment

117
Q

What are the DSM V disorders?

A

Premenstrual dysphoric disorder, binge eating disorder, mild neurocognitive disorder, somatic symptom disorder, hoarding disorder

118
Q

What are the DSM V revisions?

A

Major depressive disorder bereavement exclusion dropped
Autism spectrum disorder (Asperger’s)

119
Q

What is the international classification of diseases?

A

Comprehensive classification system for all diseases

120
Q

What are the advantages of classification?

A

Facilitating communication between researchers and clinician providing common professional language
Enables consistency in empirical research
Provides framework for discussing difficult topics and offering help
Labels helps define groups
Helps inform decisions of rational allocation of limited health services
Provides comfort and relief that they don’t feel alone

121
Q

What are the limitations of classification?

A

Some people feel disempowered by diagnosis People seen as mentally ill are often mistreated
Medicalisation of mental health problems may deflect attention from underlying social problems

122
Q

Who looked at distress of classification?

A

Horn et al, 2007

123
Q

What did Horn et al find?

A

Being seen as ‘mentally ill’ can cause more distress for some people than their original problems

124
Q

What has the DSM been criticised for?

A

Pathologising aspects of normal life
Arbituary cut offs
Insufficient attention to questions of gender and culture