Flashcards in Topic 2 Medical Model Deck (20):
-Biomedical model views disorders as being the result of biological malfunctions/disruption
-treatment reduce the effects of those malfunctions biologically through drugs, surgery etc
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.
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.
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.
-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.
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.
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
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.
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
Aim of Gottesman?
Compare vulnerability to mental illness of offspring with one or both parents having a diagnosis of schizophrenia.
-2.7million danish people
-196 couples schizophrenia; 280 children
-83 couples bipolar disorder: 146 children
-IV parental schizophrenia/Bipolar disorder-operationalised in accordance with ICD.
-DV diagnosis of any mental illness in offspring- operationalised ICD
-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%).
Both parents with serious mental illness increases the risk of their offspring developing not only that disorder but mental illness in general
Monoamines oxidase inhibitors; prevent breakdown of serotonin,Noradrenaline & dopamine so they build up
What’s Tricyclics ?
Prevent serotonin and noradrenaline being transformed after they have crossed a synapse increasing their levels
Selective serotonin reuptake inhibitors
Eg; Prozac and Seroxat
Stop serotonin being re absorbed and broken down after it arises a synapse
Noradrenaline reuptake inhibitors
Stops noradrenaline being reabsorbed and broken down after it has crossed a synapse