Component 3: Issues in Mental health - Medical Model Flashcards

1
Q

What is the medical model?

A

It views psycholigical disorders as a result of a biological malfunction or disruption. The underlying symptoms are viewed as biological in origin. It also assumes that mental disorders can be understood as illnesses in the same way that physical conditions can be. It can be classified, diagnosed and treated medically.

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2
Q

What is the biochemical explaination of mental illness?

A

One explaination for mental illness involves the possibility that symptoms are the result of abnormal neurotransmitter levels or action.

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3
Q

Explain synaptic transmission.

A
  1. An action potential travels towards the end of the pre-synaptic nuerone
  2. Vesicles move towards the membrane of the axon terminal. The neurotransmitters are released into the space.
  3. They drift across the synaptic space and bond to the post-synaptic receptors. This can trigger another action potential in the post-synaptic neurone.
  4. Neurotransmitters are reabsorbed and repackaged into vesicles. Some are broken down by the enzymes.
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4
Q

What are the two monoamine hypotheses for depression?

A

A group of neurotransmitters called the monoamines appear to be involved in depression. These include seratonin, noradrenaline and dopamine.
One version of the monoamine hypothesis says that reductions in seratonin levels, which typically follow stressful events, leads to a failure to regulate normal dopamine and noradrenaline function. This in turn disrupts mood and activity levels.
The second hypothesis says that disruption to monoamine levels is a result of abnormally high levels of an enzyme called monoamine oxidase which breaks down the monoamines, reducing their action and disrupting the passage of information around the brain

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5
Q

What are the roles of the three monoamines?

A

Depression involves lowered mood and disruption to activity levels. It is believed dopamine plays a role in regulating our mood, while noradrenaline is implicated in activity levels. Seratonin may be invloved in controlling the activity or noradrenaline and dopamine.

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6
Q

What is the genetic explanation for mental illness?

A

We randomly inherit half our genetic material from our mother and half from our father. The total genetic makeup of a person is known as the ‘genotype’. Genes are sections of DNA that contain isntructions for physical structures like the brain. It is probable that genes exert influence on individual psychological charactetistics, including mental illness, by influencing the nature of physical structures and chemical levels.
It is unlikely that mental illness is purely a resulyt of genetic factors but it does appear that some people are more vulnerable to others. Depression appears to be moderately affected by genes.

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7
Q

What is the seratonin transporter gene?

A

This gene is responsible for producing seratonin in the brain. It comes in three forms, long-long, long-short and short-short. It is believed that the short form leads to inefficient seratonin production, meaning people with this form are less resilient to the effects of stress and are more vulnerable to responding to stress with depression.

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8
Q

What is the brain abnormality explanation for mental illness?

A

Brain structure and function are associated with mental illness. E.g. some structures may develop with a different size or shape. There is evidence to show that our central nervous systems do not function normally when we suffer from certain conditions. Areas of the brain also appear to malfunction during mental disorder. Although, it is unclear whether this is simply due to abnormal neurotransmitter levels or a seperate phenomenom.

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9
Q

Explain brain abnormality relating to depression.

A

There is some evidence for brain abnormality in depression. Some studies have suggested a role for the frontal lobes, a region involved in thinking. From an MRI scan, Coffey et al that the mean frontal lobe volume in depressed patients was significantly lower than in non-depressed patients . A PET scan study by Milo et al has also shown that frontal lobes in depressed patients do not draw on blood flow in the brain as they do normally.

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10
Q

What were the aims of Gottesman’s research?

A
  1. To use a larger sample size than perivious research to investigate the likelihood of offspring being diagnosed with schitzophrenia, bipolar or another disorder if one or both parents have been diagnosed.
  2. The investigators looked at genetic links between close relatives and mental illness and to see whether genetics underlie more than one disorder
  3. They also wanted to see whether a ‘double dose’ of abnormal genes from both parents would increase the risk
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11
Q

Who were the participants in Gottesman’s study?

A

Anyone born and registered in Denmark between 1968 and 1997 (minimum of 10 years old in 2007). A sample of 2.7 million people with a register link to their mother and father.

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12
Q

What was the procedure of Gottesman’s study?

A

A longitudinal, cohort-based (secondary data) correlational study. Data on each offspring was linked with their parents psychiatric history. Using the civil registration, the researchers were able to establish who their parents were and if they were on the psychiatric register. Using the psychiatric register, the researchers identified any person with a diagnosis of schitzophrenia, bipolar or major depression.

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13
Q

What were the results of Gottesman’s study?

A
  1. If both parents were schitzophrenic, children had a 67.5% chance of having any disorder and 27.3% chance of having schitzophrenia.
  2. If both parents had bipolar, children had a 44.2% of having any disorder and a 24.95% chance of having bipolar
  3. If one parent has schitzophrenia, child has a 7% chance of also having it
  4. If one parent has bipolar, child has a 4.4% chance of also having it.
  5. If niether parent has a disorder, 11.9% chance of any disorder, 0.86% for schitzophrenia and 0.48% for bipolar
  6. If both parents have the disorder children are 31.7x more likely to have schitzophrenia and 51.9x more likely to have bipolar compared to when neither parents have a disorder
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14
Q

What were the conclusions of Gottesman’s study?

A

If both parents have a serious mental illness, then there is a significant increase in risk of their child developing not just that disorder, but other disorders.
The study supports the genetic explanation
The results may be useful for genetic cousellors helping couples planning a family.

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15
Q

What are anti-depressants?

A

Generally, anti-depressants work by raising the levels of monaoamine neurotransmitters in the brain. Monoamine oxidase inhibitors (MAOIs) prevent the breakdown of seratonin, noradrenaline and dopamine. Tricyclics prevent seratonin and noradrenaline being reabsorbed, therefore increasing their levels.

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16
Q

How effective are anti-depressants?

A

Anti-depressants are effective in reducing symptoms however, becasue they interfere with several neurotransmitters, they can have serious side effects. Newer anti-depressants tend to only work on one monoamine. E.g. SSRIs stop seratonin reabsorbtion and NRIs do the same with noradrenaline. It is important to have several anti-depressants available as individual patients vary quite a lot, both in terms of effectiveness and side effects.

17
Q

What are the side effects of anti-depressants?

A

Different anti-depressants are prescribed in different circumstances. Gender can be an issue with women suffering more side effects from tricyiclics than men. Women generally tolerate MAOIs but these are highly toxic drugs so they are not appropriate if the patient is at risk of suicide.

18
Q

What is electro-convulsive therapy?

A

ECT involves administering an electric shock for a fraction of a second to the head inducing a seizure. The seizure lasts between 15 and 60 seconds. In mmost cases it is bilateral (given to both sides of the head) as it is considered more effective

19
Q

How long is ECT carried out?

A

6-12 sessions over 2-3 weeks

20
Q

Why is ECT controversial?

A

In its early use, it was generally given without anaesthetic or muscle relaxants which sometimes resulted in broken bones or burns to the brain.

21
Q

How effective is ECT?

A

It was found that ECT is significantly more effective than drug therapy at reducing symptoms of depression. However, there is a high relapse rate with 51.1% of patients experiencing symptoms again within six months.

22
Q

What are the side effects of ECT?

A

headaches, aching muscles, dizziness and distress as well as temporary memory loss