Flashcards in Topic 2 Medical Model Deck (20):
1
Background
-Biomedical model views disorders as being the result of biological malfunctions/disruption
-treatment reduce the effects of those malfunctions biologically through drugs, surgery etc
2
Monoamines in Depression
Neurotransmitters called monoamines includes serotonin, noradrenaline &dopamine.
-Dopamine regulates our mood
-Noradrenaline is implicated in activity levels.
-Serotonin controls activity of dopamine &noradrenaline.
3
Hypothesis of monoamines in Depression
1)Reduction in serotonin levels (follow stressful events)-failure to regulate dopamine &noradrenaline-disrupts moos&activity levels.
2)Disruption of monoamines levels-High level of enzymes that breaks down monoamines-reduce their actions&disrupts the passage of information around the brain.
4
Dopamine in schizophrenia
1)Excess of dopamine in centres of the brain responsible for speech may cause hallucinations of voices.
2)Low activity of dopamine in pre frontal cortex(thinking&decision making) May explain symptoms such as apathy and incoherent thought or speech.
5
Genetic explanations?
-Genes are sections of DNA that contains instructions for producing physical structures including the brain, neurotransmitters &enzymes that breaths them down.
-it can influence the nature of physical structures of chemical level in the nervous system.
6
Genetic Vulnerability in Depression
-Stressful life events-Depression.
Genes may effect how resilient &vulnerable we are.
Eg; serotonin transporter gene comes in 3 (long-long, long-short, short-short), short-short leads to inefficient serotonin production. Less resilient to the effects is stress &are more vulnerable to respond to stress with depression.
7
Genetic vulnerability in schizophrenia
-Can be genetically influenced-family member.
-polygenic- influenced by over 100 genes
-aetiologically heterogeneous- different combination of factors can lead to similar symptoms
8
Brain abnormality in Depression
-Studies suggested frontal lobe is involved in thinking.
1)Coffey et al-mean frontal lobe volume in depressed patient smaller.
2)milo et al-frontal lobe in depressed patients don’t draw on blood flow in the brain as they normally do-hyper fusion.
9
Brain abnormalities in schizophrenia?
1)Pardon et al-Involves problem with left hemisphere.
2)jackel et al-Negative correlation between activity levels in ventral striatum&severity of negative symptoms.
3)Allen at al-Low activation levels in superior temporal gyrus &anterior cingulate gyrus- Hallucinations
10
Aim of Gottesman?
Compare vulnerability to mental illness of offspring with one or both parents having a diagnosis of schizophrenia.
11
Sample
-2.7million danish people
-196 couples schizophrenia; 280 children
-83 couples bipolar disorder: 146 children
12
Design
Cohort study
Natural experiment
13
IV&DV?
-IV parental schizophrenia/Bipolar disorder-operationalised in accordance with ICD.
-DV diagnosis of any mental illness in offspring- operationalised ICD
14
Results
-schizophrenia & bipolar diagnosis by BOTH parents increased chance of offspring getting a diagnosis(27.3% schizophrenia &24.95% bipolar).
-diagnosis for mental illness in general (schizophrenia 67.5% &44.2%).
15
Conclusion
Both parents with serious mental illness increases the risk of their offspring developing not only that disorder but mental illness in general
16
What’s MAOI’s?
Monoamines oxidase inhibitors; prevent breakdown of serotonin,Noradrenaline & dopamine so they build up
17
What’s Tricyclics ?
Prevent serotonin and noradrenaline being transformed after they have crossed a synapse increasing their levels
18
What’s SSRI’s?
Selective serotonin reuptake inhibitors
Eg; Prozac and Seroxat
Stop serotonin being re absorbed and broken down after it arises a synapse
19
What’s NRI’s?
Noradrenaline reuptake inhibitors
Stops noradrenaline being reabsorbed and broken down after it has crossed a synapse
20