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PS1110 > The biomedical model > Flashcards

The biomedical model Flashcards

1
Q

what do models in psychology do?

3 points

A

models spell out:
* basic assumptions
* give order to the field under study
* provides a structured framework for scientific investigation

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2
Q

mental health models

what do models influence

4 points

A
  • what investigators observe
  • the questions they ask
  • the information they seek
  • how they interpret the data
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3
Q

what is the biological model

what does the biological model of metal disorders adopt?

A

a medical or biological perspective

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4
Q

biological model assumptions?

3 assumptions

A
  • mental disorders are biologically-based brain diseases
  • the underlying cause is organic
  • mental disorders reflect a disturbance of brain structure and/or function
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5
Q

what is the biological model?

A

the biological model argues that there is no meaningful distinction between mental and physical disease

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6
Q

from the 1970s what was maladaptive behaviour?

A

maladaptive behaviour increasingly considered to be a function of an interaction between biological, psychological and social factors

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7
Q

the biological model today

metal disorders

A

the idea that mental disorders are biologically-based brain diseases remains very influential

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8
Q

the biological model today

pharmacological agents

A

the biological model reflected the increase use of pharmacological agents in mental illnesses (e.g. depression, anxiety)

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9
Q

the biological model today

research evidence

A

there is a large body of research evidence correlating mental functions and brain activity

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10
Q

mental disorders: biological causes

neurotransmitter imbalance: altered production (or release)

A

altered production (or release) of neurotransmitter at synapses, over-or under-stimulating the target neuron

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11
Q

mental disorders: biological causes

neurotransmitter imbalance: altered reuptake (or degradation)

A

Altered reuptake (or degradation) of neurotransmitters, increasing or decreasing concentration at synapses

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12
Q

mental disorders: biological causes

neurotransmitter imbalance: alterations in neurotransmitter receptors

A

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

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13
Q

mental disorders: biological causes

psychotropic drugs

A

many drugs used to treat mental health disorders act at central (brain) synapses by increasing or decreasing neurotransmission at particular synapses

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14
Q

mental disorders: biological causes

what do psychotropic drugs influence?

A

psychotropic drugs used in the treatment of mental disorders influence synaptic transmission

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15
Q

mental disorders: biological causes

psychotropic drug mechanisms

3 points

A

mechanisms:
1. increased or decreased transmitter synthesis/release
2. increased or decreased transmitter re-uptake/inactivation
3. direct stimulation or inhibition of transmitter receptors

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16
Q

drugs and mental disorders

A

some drug discovery sheds light on mechanisms of disease - or understanding disease mechanisms allows rational drug design

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17
Q

amine hypothesis of depression

resperpine (drug)

A

in the 1950s the drug resperpine was approved to treat high blood pressure. but some patients appeared to become depressed or suicidal

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18
Q

amine hypothesis of depression

what was the drug resperpine doing to the body?

A

the drug was found to work by depleting nerve cells of amine neurotransmitters (e.g. seratonin & dopamine)

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19
Q

amine hypothesis of depression

iproniazis (drug)

3 points

A
  • late 1950s - anti-tuberculosis drug developed (iproniazis)
  • side-effects: euphoria, increased apetite and improved sleep
  • it increased amine neurotransmitters - used to treat depression
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20
Q

amine hypothesis of depression

what is depression caused by?

A

deficiency of amine neurotransmitters

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21
Q

how do anti-depressants work?

A

they work by correcting brain ‘amine deficiency’

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22
Q

amine hypothesis of depression

what are most antidepressants?

A
  • serotonin-selective reuptake inhibitors (SSRIs)
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23
Q

amine hypothesis of depression

what does blocking re-uptake of serotonin do?

A

increases its concentration at the synapses in the brain

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24
Q

amine hypothesis of depression

what was the most perscribed drug in the US

A

Zoloft (sertraline)

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25
Q

criticism of the amine hypothesis

oversimplification

4 points

A
  • methodological problems
  • inconsistent findings
  • discredited serotonin hypothesis
    very small sample sizes, poor control of confounding variables
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26
Q

other mental health disorders

depression

A

symptoms due to deficiency of monoamine transmitters: noradrenaline, serotonin

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27
Q

other mental health disorders

schizophrenia

A

core psychotic symptoms such as delusions and hallucinations are due to excess brain dopamine

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28
Q

other mental disorders

obsessive-compulsive disorder (OCD)

A

symptoms caused by dysfunction in brain pathways regulated by serotonin

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29
Q

biological models are complex

issues with accounts of biological models of disease:

A

they are often highly simplistic and misleading

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30
Q

biological models are complex

issues with biological disease models:

A

they are highly complex and sophisticated and are supported by extensive research evidence spanning many decades:
* genetics
* structural and functional brain imaging
* autopsy and neurodevelopmental studies
* animal models

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31
Q

hormones in mental disorders

what does the endocrine system consist of?

A

glands that secrete hormones into the bloodstream

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32
Q

hormones in mental disorders

what are hormones?

A

chemical messengers that control bodily functions (e.g. sex, feeding)

33
Q

hormones in mental disorders

what is the piturity gland?

A

the ‘master gland’ of the endocrine system

34
Q

hormones in mental disorders

what is the piturity gland controlled by?

A

hypothalamus

35
Q

hormones in mental disorders

hypothalamic-piturity-adrenal (HPA) axis

A
  • over-active in stress, including chronic psychological stress
  • leads to persistent elevation of the stress hormone cortisol in the bloodstream
  • implicated in several psychological disorders (e.g. depression, anxiety)
36
Q

genetic vulnerability

chromosomal abnormalities

A

complete or partial duplications/deletions (e.g. down syndrome: intellectual disability/dementia)

37
Q

genetic vulnerability

single gene defects

A

abnormalities in particular genes (mutations) or disease associated normal variants (polymorphisms)

38
Q

what are vulnerabilites to mental disorders?

A

they are ususally polygenic (influenced by multiple genes)
* there is not usually a single gene for a particular mental disorder

39
Q

epigenetics

what are epigenetics?

A

when a person’s genetic code is fixed at birth, but genes can be switched ‘on’ or ‘off’ during life

40
Q

epigenetics

how are genes silenced?

A

by adding molecular tags (methyl groups) to parts of the DNA strand

41
Q

epigenetics

how is the pattern of gene methylation influenced?

A

it is influenced by the environment including early life experiences

42
Q

epigenetics

what can adverse life experiences lead to

A

adverse life experiences (e.g. bullying, neglect) can lead to epigenetic changes that influence risk of mental health disorders in adulthood

43
Q

gene-environment interaction

behaviour is not exclusively determined by?

A

the genes you inherit
* psychiatric disease risk depends on both genetic and environmental factors

44
Q

biological model: treatment

AIM

A

target the underlying biological dysfunction

45
Q

biological model: treatment

ULTIMATE GOAL

A

discover precise therpeutic agents that the target disease process without causing harm

46
Q

biological model: treatment

MOST TREATMENTS

A

pharmacological

47
Q

biological model: treatment

OTHER TREATMENTS

A

brain stimulation, surgery

48
Q

insulin shock therapy

who created the insulin shock therapy?

A

Manfred Sakel (1933)

49
Q

inslulin shock therapy

what was insulin shock therapy used for?

A

mainly used for schizophrenia in the 1940s and 1950s

50
Q

insulin shock therapy

risks of insulin shock therapy:

A

obesity, seizures, brain damage or death

51
Q

prefrontal leukotomy

who created prefrontal leukotomy?

A

Egaz Moniz

52
Q

frontal lobotomy

who created frontal lobotomy?

A

Walter Freeman who performed 3500 lobotomies

53
Q

frontal lobotomy

what did frontal lobotomy do?

A

reduced emotional distress and improved challenging behaviour but left patients ‘flat’, passive and unemotional

54
Q

electroconvulsive therapy (ECT)

what was ECT?

A

controlled induction of convulsive seizured under general anaesthesia

55
Q

ECT

what does ECT affect?

A

affects numerous neurochemical (neurotransmitter) systems

56
Q

deep brain stimulation

stimulation of area 25

A

stimulation of area 25 in the limbic lobe of the brain is associated with dramatic mood improvement in severe depression

57
Q

DBS

what is deep brain stimulation used for?

A

used for severe treatment-resistant conditions (e.g. depression, OCD)
* very expensive and carries risks associated with neurosurgery

58
Q

transcranial magnetic stimulation (TMS)

what is transcranial magnetic stimulation used for?

A

used for treatment-resistant depression and anxiety disorder

59
Q

transcranial magnetic stimulation (TMS)

how does TMS work?

A

electromagnetic coil delivers magnetic pulses to the brain - exact mechanism of action unclear

60
Q

pharmacological treatments

psychotropic agents

A

any medication capable of affecting the mind, emotions and behaviour

61
Q

pharmacological treatments

what are the most common forms of medical treatment for mental disorders?

4 points

A
  • antidepressants (low mood)
  • anxiolytics (anxiety)
  • antipsychotics/neuroleptics (psychosis)
  • mood stabilisers (bipolar disorder)
62
Q

antidepressant agents

several types, acting on different neurotransmitters:

A
  • patients do tend to improve
  • side effecis: nausea, nervousness, insomnia, sexual dysfunction
63
Q

antidepressant agents

commonly perscribed antidepressants:

4 types

A
  • fluoxetine
  • sertraline
  • paroxetine
  • citalopram
64
Q

anti-anxiety drugs (anxiolytics)

when are anxiolytics used?

A

they are used if guided self-help and cognitive-behavioural therapy fails

65
Q

anti-anxiety drugs (anxiolytics)

anxiolytics examples:

A

benzodiazepines (valium, xanax)
* sedative and muscle relaxing properties
* causes drowsiness and lethargy
* highly addictive, high relapse rates

66
Q

antipsychotic drugs (neuroleptics)

what are neuroleptics used for?

A

they are used to treat psychotic disorders and act by blocking brain dopamine (and/or serotonin) receptors
* effective in reducing delusions and hallucinations

67
Q

mood stabilisers

what is lithuim used for?

A

used to treat bipolar affective disorder

68
Q

KEY POINTS: biomedical model

3

A
  • biomedical model assumes that disorders have an organic or physical cause
  • many treatments have been based in the biomedical model, of which some are now discredited
  • treatments fall into 3 main categories: drugs, surgery and brain stimulation
69
Q

KEY POINTS: Pharmacological interevntions

3 points

A
  • pharmacological interventions are by far the most common
  • they have revolutionalised the management and care of people with mental illnesses
  • however, they are not cures
70
Q

biomedical approach: advantages

biomedical approach advantages:

3 points

A
  • suggests clear mechanism for most disorders: obvious improvement on ‘supernatural’ explanations
  • effective in delivering insights into disorders with a clearer biological base (e.g. alzheimer’s disease)
  • drug treatment has revolutionised patient care: it is generally effective (and faster) than other therapies
71
Q

biological approach: advantages

treatment based on the scientific method

A

in theory this means treatments should only be adopted if proven effective
For example: antidepressants
* Meta analysis suggested SSRI antidepressants were no more effective than placebo, except in severe cases
* But another showed that patients are either responders or nonresponders

72
Q

research evidence: explained

randomised control trial

A

ideally it should be ‘double blind’ RCT so that neither patient nor researcher know who is in the treatment (vs. placebo) groups

73
Q

research evidence: explained

importance of meta analysis

A

a meta-analysis can be used to pool results from multiple trials

74
Q

biomedical approach: limitations

assumes universality

A
  • no room within its framework for social, psychological, or behavioural dimensions of disorders
  • causality: cause by-product of disorder?
  • redctionism: is psychology really biology?
75
Q

biomedical model: controversy

CLAIM: Mental disorders are brain diseases caused by
neurotransmitter dysregulation, genetic anomalies, and defects in brain structure and function

A

Yet, scientists have not identified a biological cause of, or even a reliable biomarker for any mental disorder

76
Q

biomedical model: controversy

CLAIM: Psychotropic medications work by correcting the
neurotransmitter imbalances that cause mental disorders

A

However, there is no credible evidence that mental disorders are caused by chemical imbalances, or that medicines work by correcting such imbalances

77
Q

biomedical model: controversy

CLAIM: Biological psychiatry has made great progress in reducing the societal burden of mental disorder

A

However, mental disorders have become more chronic and severe, and the number of individuals disabled by their symptoms has steadily risen in recent decades

78
Q

biomedical model: controversy

CLAIM: Educating the public that mental disorders are biologicallybased medical diseases reduces stigma

A

But, despite the public’s increasing endorsement of biological causes and treatments, stigma remains and shows signs of worsening

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