Mental Health Topic 2 Flashcards

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1
Q

What is the medical model?

A

Explains mental disorder due to physical causes such as:
Brain structure,
genetics and biochemistry.

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2
Q

How is the medical model deterministic?

A

as it emphasizes that a person has no more free choice or control over a mental disorder than a physical illness.

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3
Q

Is the medical model restuctionist or holistic?

A

The medical model is reductionist as it oversimplifies causes of mental illness, ignoring psychological and environmental factors. In the other hand, recent biological explanations are looking at complex interactions between genes and environment, therefore becoming more holistic.

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4
Q

What is the basic biochemical principals?

A

-Brain cells transmit information in the form of electrical impulses around the brain.
-Between brain cells are gaps (synapses)
-For info to pass from one cell to the next, neurotransmitters must pass across the synapse.
-different neurotransmitters are important in different parts of the brain and are believed to be important in regulating different mental processes.
-One explanation for MI is the possibility that symptoms are due to abnormal neurotransmitter levels or action.

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5
Q

What is the monamine hypothesis?

A

Low levels of certain monamines which are a group of neurotransmitters that regulate mood can cause MI.

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6
Q

What does serotonin do?

A

Regulates the other neurotransmitters. Without this regulation, brain functioning becomes erratic. When serotonin levels drops so does noradrenaline’s and dopamine’s

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7
Q

What does noradrenaline do?

A

Is needed for alertness and low levels can be linked to a lack of pleasure.

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8
Q

What does dopamine do?

A

Related to alertness, energy, motivation and to feel pleasure/rewards Low levels of dopamine are linked to anxiety.

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9
Q

How is the gene 5-HTT linked to depression

A

Linked to regulating serotonin levels. People with variations to the 5-HTT gene that are under-active seem more likely to suffer from depression after stressful life events.

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10
Q

How is the chemical MAO-A linked to depression?

A

Removes monamines from the synapse. This is an important brain function called “re-uptake” that recycles neurotransmitters when they don’t appear to be needed. If there is too much MAO-A in the synapse, it will remove monamines that are needed, starving the brain of serotonin, noradneranaline and dopamine leading to symptoms of depression.

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11
Q

What is the basics for anti-depressant drugs?

A

Inhibit the activity of MAO-A. This leads to more monamine activity and a reduction in the symptoms of depression.

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12
Q

What is the genetic explanation of mental illness?

A

genetic inheritance may determine features of our behavior, appearance, personality and achievements. Genes may also influence individual psychological characteristics including metal illness

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13
Q

What are concordance rates?

A

Similarities between two relatives can be measured using a term concordance rat yes. a researcher would compare people that are genetically related on a basis of weather they have the same disorder.

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14
Q

What are the family studies?

A

Family studies commonly show relationships between tarits and inheritance. Family studies tend to compare first-degree relatives to individuals and assess concordance rate. you would expect higher CR for first-degree relatives.

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15
Q

What are the twin studies?

A

A quasi experiment in which we compare CR for identical (monozygotic) and non identical twins (dizygotic). You would assume that MZ twins have higher CR due to the fact they are genetically identical. However twins are often brought up in the same environment.

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16
Q

What are the adoption studies?

A

Individuals who have been adopted as children are assessed in terms of characteristics and compared to biological and adoptive parents. Genetic factors are involved if CR are higher amongst biological relatives compared to adoptive relatives.

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17
Q

What did Allen (1976) find?

A

CR for MZ twins and depression was 40% but this falls to 11% for DZ twins, providing evidence for genetic contribution to depression.

18
Q

What did Wender et al find?

A

Showed clear evidence for genetic effects. they found that biological relatives of a depressed adoptee were eight times more likely that adoptive relatives to also have depression.

19
Q

What is the brain abnormality explanation?

A

Refers to how a mentally ill patient’s brain is different from a neuro-typical person’s brain, or how their brain differs from when they were mentally healthy. Focuses on abnormality of the structure in the brain rather than biochemical abnormalities.

20
Q

What is the prefrontal cortex responsible for?

A

beahavioural control- damage causes issues with self-control and emotional processing.

21
Q

What is the amygdala responsible for?

A

Feelings of fear and emotional memory storage.

22
Q

What is the hippocampus responsible for?

A

processing memories and responding to stress hormones. When damaged associated with memory loss.

23
Q

What scans are used to investigate brain differences?

A

PET and MRI

24
Q

what happens to the hippocampus with depression?

A

May cause it to shrink or weaken.
Repeated stress may cause neurons in the hippocampus to shrink.

25
Q

What happens to the pre frontal cortex in depressed patients?

A

Shrink

26
Q

What happens to the amygdala in a depressed patient?

A

Increases in activity have been found when depressed patients are presented with a negative stimuli such as a sad face. but reduced activity when presented with a positive stimuli.
Suggests that the amygdala of depressed patients does not process facial stimuli in a way that healthy individuals would do.
Since the Amygdala regulates emotion it makes sense that it s implemented in depression.

27
Q

What was the aim of Gottesman’s study?

A

To investigate weather two parents with MI would increase the probability that their child would also be diagnosed with a mental disorder.

28
Q

What method was used in Gottesman’s study?

A

national cohort study
Quasi experiment

29
Q

What was the IV and DV of Gottesman’s study?

A

IV-Parental SZ/BP (using ICD 8 or 10)
DV-offspring diagnosis of any mebnatl illness.

30
Q

What was the sample in Gottesman’s study?

A

2.7 million danish people born before 1997
sampled in 2007
No consent was needed as data gathered was from public domain and names were anonymous.
A sample was taken from this population of:
-196 couples of whom has SZ and their 270 children
-83 couples both diagnosed as bipolar and their 146 children.
They also took sample of families where only one parent had a diagnosis.
and recorded the rest where neither had a diagnosis.

31
Q

What were some results for Gottesman’s study?

A

Risk of SZ with two parents= 27.3% and for any MI=67.5%
Risk of SZ with one parent=7% and for any MI=11.9%
For ps with neither=1.12% and for any 14.1%

32
Q

what does a re uptake inhibitor do?

A

Prevents the process in which neurotransmitters are naturally reabsorbed into nerved cells in the brain after they are released to send messages between nerve cells.
A re uptake inhibitor prevents this so instead of getting reabsorbed the neurotransmitter stays in the gap between the nerves called the synapse.

33
Q

What is an example of a re uptake inhibitor?

A

selective serotonin re-uptake inhibitors (SSRIs) which are some of the most commonly prescribed antidepressants available. They include Celexa, Lexapro, Luvox, Paxil, prozac and Zoloft

34
Q

What has research shown about the serotonin transporter gene? (Weinberger et al)

A

Shows that this gene is responsible for producing a nerurotranmitter called serotonin which has been implicated in depression.
Weinberger et al found that this gene has 3 forms, long-long, long-short and short-short. the short form leads to inefficient serotonin production: brain scan studies showed people with this variant react more negatively to emotional stimuli. this suggests that tehy will not be able to handle stressful life events as well as others and therefore are more vulnerable to responding to stress with depression.

35
Q

What did Thompson et al do and find in relation to the hippocampus?

A

MRI scan from 9,000 people in 7 countries was collected. Of those, just over 1700 had a clinical diagnosis of major depression and 7200 were a control he found:
Depressed people had a smaller hippocampus than non-depressed people
These brain differences become more severe the longer an individual suffers from depression as well as in people who receive a diagnosis of depression at an early age.

36
Q

What did Sheline (2001) find in relation to the amygdala?

A

Found that in an fMRI scan of 11 depressed patients and control. The scan showed that the amygdala was more active in the depressed patients both during “resting” states and when exposed to emotional stimuli such as images showing fear. When the depressed patients were given antidepressants there was a reduction in activity in the amygdala.

37
Q

What is reuptake and a reuptake inhibitor?

A

It’s the process in which neurotransmitters are naturally reabsorbed back into nerve cells in the brain after they are released to send messages between nerve cells. A reuptake inhibitor prevents this from happening. Instead of getting reabsorbed, the neurotransmitter stays in the gap between the nerves, called the synapse.

38
Q

What’s the benefit of reuptake inhibitors?

A

The basic theory goes like this: keeping levels of the neurotransmitters higher could improve communication between the nerve cells- and that can strengthen circuits in the brain which regulate mood.

39
Q

What are some examples of reuptake inhibitors?

A

Selective serotonin reuptake inhibitors are some of the most commonly prescribed antidepressants available. they include Celexa, Lexapro, Luvox, Paxil, Prozac and Zoloft

40
Q

What did Arroll et al find about the usefulness about drug treatments?

A

60% of patients treated with antidepressants improved compared to 47% with placebo.

41
Q

What are some problems with drug treatment?

A

Drugs only alleviate the symptoms of disorders. As soon as the patients stop taking the drugs the symptoms return.
All drugs have side effects! Anxiety, sexual dysfunction, insomnia, nausea, suicidal thought etc.
Dependence
Not effective for all
The effectiveness of antidepressants does not mean the sole cause of the depression is biochemical.

42
Q

What is the conclusion of Gottesman’s study?

A

Having both parents with a serious mental illnes is associated with a sig increased risk of developing mot only that disorder but mental illness in general, Having one parent with a serious mental illness carries a bit of risk. this provides useful information for genetic counselling which involves advising people of their own risks of developing illness or passing it on genetic vulnerability to their children.