Mental Health - Area 2 Flashcards

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1
Q

What does the biochemical principle focus on ?

A

Focusses on abnormal levels of neurotransmitters.

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2
Q

What are excitatory neurotransmitters ?

A

Causes the next neurone to be activated (over stimulated)

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3
Q

What are inhibitory neurotransmitters ?

A

Prevents action of the next neurone.

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4
Q

What does the monoamine hypothesis of depression state ?

A

Proposes that depression is caused by levels of monoamines, a group of neurotransmitters.

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5
Q

What neurotransmitters does monoamines include ?

A

Serotonin, dopamine and noradrenaline (in hippocampus and hypothalamus responsible for heart rate.

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6
Q

What was Meyer’s study in 2006 ?

A

Studied 17 patients with depression, who had not taken antidepressants for 5 months and used PET scan to compare with 17 clinically normal patients.

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7
Q

What did Meyers (2006) find ?

A

Found that depressed patients had significantly higher levels of monoamine oxidase in all 11 brain regions. (Causes monoamines to brake down too quickly).

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8
Q

What does the dopamine hypothesis of schizophrenia state ?

A

States that an excess of dopamine at limbic system causes schizophrenia.
The revised hypothesis is that there is an excess of dopamine at D2 receptors.

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9
Q

What are positive symptoms of schizophrenia linked with ?

A

Linked with hypo function (too much dopamine activity) in mesolimbic pathway, which is responsible fore motivation, emotion and reward.

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10
Q

What are negative symptoms of schizophrenia linked with ?

A

Linked with erratic dopamine function in mesocortical pathway, which is responsible for executive function.

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11
Q

What did Seeman (1987) study ?

A

Looks at several stands of evidence that provides support for dopamine hypothesis.

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12
Q

What did Seeman (1987) find ?

A

-Drugs increase levels of dopamine increase symptoms of schizophrenia.
-Antipsychotics reduce schizophrenia symptoms.
-Post mortem of schizophrenia brains have increased density of D2 receptors than normal patients.

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13
Q

What is GABA ?

A

They are important inhibitory neurotransmitters in CNS. They switch off next neurone, reducing activity.

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14
Q

What is GABA responsible for in biochemical explanation of mental health ?

A

Counterbalances glutamate neurotransmitters. People with phobias have decreased levels of GABA so neurone in glutamate pathway is increased leading to anxiety.

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15
Q

What did Panda et al (1999) look at ?

A

Assigned 69 patients with social phobia, where they took a drug that increased levels of GABA for 14 weeks and gave control group placebo.

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16
Q

What did Panda et al (1999) find ?

A

Found significantly lower symptoms in GABA group, suggesting that increased levels of GABA can lead to a reduction in anxiety.

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17
Q

What does the brain abnormality of depression state ?

A

States that Limbic system shows differences in amount of grey matter and levels of activity in the brain (amygdala and hippocampus).

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18
Q

What does brain abnormality of depression in amygdala state ?

A

Increased activity in amygdala when depressed patients were presented with a negative stimuli. However, there was reduced activity when depressed patients were presented with a positive stimuli.

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19
Q

What does brain abnormality of depression in hippocampus state ?

A

Hippocampus is significantly smaller in patients with depression (reduced by 20%). The more severe the depression, the more severe the loss of grey matter in the hippocampus.

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20
Q

What did Sheline (2001) study in terms of amygdala ?

A

Gave FMRI scans to 11 depressed patients and 11 control patients.

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21
Q

What did Sheline (2001) find in terms of amygdala ?

A

Found that amygdala was more active in patients with depression that control group during resting and activity when shown emotional images expressing fear.

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22
Q

What did Kronmuller (2008) study in terms of hippocampus size ?

A

Found that significantly smaller hippocampus in 33 females and 24 males, who relapsed over 2 years of being treated compared to control group of 30 healthy individuals. Males showed volume of hippocampus is linked with a person more likely to experience depression.

23
Q

What does brain abnormality of schizophrenia state ?

A

People with schizophrenia have enlarged ventricles. Ventricles do not have nay cognitive function.
Over smaller brain in patients with schizophrenia but reduction stops when taking antipsychotics.

24
Q

What does loss of grey matter in temporal lobe explain in terms of schizophrenia ?

A

Explains auditory hallucinations.

25
Q

What does loss of grey matter in frontal lobe explain in terms of schizophrenia ?

A

Explains in coherent speech and delusions.

26
Q

What does loss of grey matter in thalamus explain in terms of schizophrenia ?

A

Leads to auditory and verbal hallucinations.

27
Q

What did Pol et al (2002) study ?

A

Studied 159 patients with schizophrenia compared with 158 healthy patients.

28
Q

What did Pol et al (2002) find ?

A

Found that there is a 30% increase in size of ventricles of ppts with schizophrenia. The larger the ventricles, leads to decreased amounts of grey matter so decreases functionality.

29
Q

What brain abnormality in prefrontal cortex causes phobias ?

A

It suppresses fear response, but if this fails, it fails to suppress urges from amygdala causing anxiety/phobia.

30
Q

What brain abnormality in amygdala causes phobias ?

A

Detects and responds to threats in environment. People with phobias have smaller amygdala with increased blood flow, which is associated with inability to control behaviour and physiological responses to fearful objects.

31
Q

What brain abnormality in hippocampus causes phobias ?

A

Associated with memory. Decrease in hippocampal function means a person only recalls link with stimulus and previous fearful experience rather than neutral or positive feelings.

32
Q

What did Ahs et al (2009) study ?

A

Used PET scans to measure cerebral blood flow in amygdala and prefrontal cortex of patients with snake or spider phobia.

33
Q

What did Ahs et al (2009) find ?

A

Found increased activity in amygdala and reduced activity in the prefrontal cortex.

34
Q

What is the genetic explanation of depression using family studies ?

A

Gottesman showed and increased risk of children having bipolar if their parents have that or another disorder.

35
Q

What is the genetic explanation of schizophrenia using family studies ?

A

There is a 1% risk of schizophrenia but the risk is 10x greater for first degree relatives of a person with schizophrenia.

36
Q

What is the genetic explanation of phobias using twin studies ?

A

Kendler (1992) found concordant results for animal type specific phobias that were 25.9% for monozygotic twins and only 11% for dizygotic twins implying a genetic causation.

37
Q

Background to Gottesman

A

-Krapelin + Bleuler found morbid risk of offspring of both parents with schizophrenia was 28-58%.
-Risk of manic disorder was 22-80%, which is x2-x4 risk just one parent with schizophrenia.

38
Q

Aim of Gottesman

A

To find out if the offspring of families, where both parents had severe mental illness were more likely to experience a sever mental disorder.

39
Q

Method of Gottesman

A

Conducted in Denmark using a natural experiment
IV= parents with diagnosis of schizophrenia or bipolar
DV= offspring receiving diagnosis.

40
Q

Sample of Gottesman

A

Population based cohort of 2.7 million people born in Denmark, alive or born after 1968. Restricted to people aged 10 or over before January 1st 2007.

41
Q

Sample of both parents with schizophrenia in Gottesman

A

196 couples with both parents with schizophrenia and their 270 children.

42
Q

Sample of both parents with bipolar in Gottesman

A

83 couples both with bipolar disorder and their 146 children.

43
Q

Sample of comparison group with one parent with schizophrenia in Gottesman

A

8006 couples with 1 parent is diagnosed with schizophrenia and approx 14,000 children.

44
Q

Sample of comparison group with one parent with bipolar in Gottesman

A

Comparison group of 11995 couples, where one parent is diagnosed with bipolar and approx their 23000 children.

45
Q

Results of both parents with schizophrenia in Gottesman

A

27.3% diagnosis in children of 196 couples both with schizophrenia.

46
Q

Results of both parents with bipolar in Gottesman

A

24.9% risk of bipolar of 83 couples both diagnosed with bipolar.

47
Q

Results of one parent with schizophrenia in Gottesman

A

7% diagnosis of schizophrenia in offspring when 1 parent has schizophrenia.

48
Q

Results of one parent with bipolar in Gottesman

A

4.4% diagnosis of bipolar in offspring when one parent has bipolar.

49
Q

Results of one parent with schizophrenia and one parent with bipolar in Gottesman

A

15.6% when one parent has bipolar and one has schizophrenia. There is an 11.7% maximal risk of any disorder.

50
Q

Results of no parents with a psychotic disorder in Gottesman

A

General population with parents with no psychiatric admission, the cumulative incidence was 14.1% so 1 in 7 were admitted by age of 52 years.

51
Q

Conclusions of Gottesman

A

Offspring of both parents having psychosis have a high risk of diagnosis of psychosis.
Evidence to support genetic explanation.
Derived risk of psychosis may lead to counselling.

52
Q

Drug therapy application of depression (5 marks)

A

Drug therapy is used to treat depression through use of antidepressants, such as SSRI, which are taken in tablet form. They stop serotonin being reuptaked at pre-synaptic neurone so it is absorbed at post synaptic neuron. This increases the individual’s mood.

53
Q

Drug therapy application for schizophrenia (5 marks)

A

Drug therapy is used to treat schizophrenia through use of antipsychotics, such as atypical antipsychotics, that target both positive and negative symptoms of schizophrenia. They work by blocking some of the D2 receptors at the post-synaptic neurone. This reduces the amount of dopamine absorbed at the D2 receptors causing less overstimulation of post-synaptic neurone so remains in the synaptic gap.

54
Q

ECT therapy application for depression (5 marks)

A

ECT is used to treat depression through use of electrical waves through brain to cause seizure to make patient calm. Can be unilateral or bilateral to one or both temples. They are thought to work by electrical waves stimulating serotonin to reduce depressive symptoms in patients, so patients receive higher levels of serotonin at post synaptic neurone.