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Biological Psychology 2 > Mental Illnesses: Anxiety Disorders & Schizophrenia > Flashcards

Mental Illnesses: Anxiety Disorders & Schizophrenia Flashcards

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1
Q

What is the Biopsychosocial approach?

A

How Biology, Psychology, Social context and Health all interact together.

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2
Q

How prevalent is SP?

A

1%. Most common in males.

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3
Q

What was SP originally named?

A

Dementia praecox (Kraepelin).

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4
Q

Who named it SP?

A

Bleuer.

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5
Q

Name 4 positive symptoms of SP?

A

Delusions, hallucinations, disorganised speech, disorganised behaviour.

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6
Q

Name 4 negative symptoms of SP?

A

Reduced expression of emotion, neglect of personal hygiene, poverty of speech, difficulty initiating goal-directed behaviour.

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7
Q

What are relapses and remissions?

A

Symptoms get worse.

Symptoms get better.

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8
Q

What is a psychotic episode?

A

A period of intense positive symptoms.

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9
Q

Name 3 cognitive symptoms of SP.

A

Poor ability to maintain attention, impaired verbal working memory, inflexible thinking style.

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10
Q

Name some disorders SP is similar to?

A

Mood disorders with psychotic features, substance abuse, brain damage, Huntington’s, Alzheimer’s.

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11
Q

What causes SP?

A

Genetics + environment.

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12
Q

High or low heritability?

A

High.

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13
Q

What is the likelihood of an identical twin of someone with SP also having it?

A

48%.

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14
Q

How many genes are implicated in SP?

A

+100 high risk genes.

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15
Q

Name one way in which more mutations can occur?

A

Increased paternal age at conception.

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16
Q

Explain the gene-environment interaction?

A

Environment might lead to certain gene expression/some genotypes.

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17
Q

What is the factor most important in neurodevelopment?

A

Prenatal factors.

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18
Q

What other factor can increase the risk?

A

Cannabis in adolescence.

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19
Q

Name the 3 main brain abnormalities in SP.

A

Larger ventricles - increases as disease develops.
Less grey + white matter.
Less brain connectivity.

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20
Q

Why is there some controversy over the brain abnormalities in SP?

A

Researchers are unsure if it is cause or effect.
Medication could be affecting this.
High risk groups show some differences before diagnoses.

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21
Q

Give an example of when brain abnormalities were seen prior to diagnosis (SP).

A

Synaptic over-pruning in the prefrontal cortex.

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22
Q

What does a white matter reduction lead to?

A

Disrupted communication in the brain.

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23
Q

What is interesting about the corpus callosum volume being reduced in SP?

A

It can also be seen in relatives - shows genetic influence.

24
Q

Do SP have lower or higher brain connectivity?

A

Lower.

25
Q

Explain the dopamine hypothesis.

A

SP is the result of excess activity at dopamine synapses in certain regions. Neurons release dopamine faster than average.

26
Q

What is the evidence for the dopamine hypothesis?

A

All antipsychotic drugs act on dopamine.
4/10 of the top gene variants associated with SP are involved in dopaminergic pathways.
Some dopaminergic recreational drugs cause hallucinations and delusions.
PET studies - higher levels of dopamine synthesis and release in the striatum.
Neuroleptic drugs block D2-receptors. Leads to improved positive symptoms. There is a threshold amount of D2 binding for the treatment to work.

27
Q

What are some side effects of D2-receptor blocking?

A

Extrapyramidal symptoms.

Very fine line between improvement + side effects.

28
Q

What is the threshold of receptor binding that can occur before having side effects?

A

80%.

29
Q

What are typical antipsychotics like?

A

Act on D2 receptors. Neuroleptics. High incidence of side effects on motor control.

30
Q

What are atypical antipsychotics like?

A

Act on several receptor (D2, D3, D4) + serotonin. Reduced risk of motor control side effects but causes drowsiness, weight gain…

31
Q

What are some limitations of the dopamine hypothesis?

A

1/3 of people don’t respond to antipsychotics.
Relationship between dopamine and negative and cognitive symptoms is unclear.
Substance dependence.

32
Q

Explain the glutamate hypothesis.

A

Schizophrenia is due to NMDA receptor dysfunction.

33
Q

What is the evidence for the glutamate hypothesis?

A

Ketamine and PCP contain NMDA receptor antagonists which show side effects that resemble +, - and cognitive symptoms. Symptoms worsen in SP.
Mice treated with PCP show same behavioural patterns as mutant mice. Mice models too simple for studying SP?

34
Q

Why is there some controversy regarding the glutamate hypothesis?

A

Treatments have not shown conclusive/strong effects.

There is close interactions between glutamate and dopamine (e.g. ketamine acts on dopamine release too).

35
Q

What is NMDA dysfunction most likely to contribute to?

A

Negative symptoms.

36
Q

Define anxiety disorders.

A

A deviant, distressful and dysfunctional pattern of thoughts, feedings or behaviours that interferes with the ability to function in a healthy way.

37
Q

What are the 5 main anxiety disorders identified by DSM-V?

A

Specific phobia, social anxiety disorder, generalised anxiety disorder, panic disorder, agoraphobia.

38
Q

What are panic attacks?

A

A feeling of sudden and intense fear and anxiety. <30 minutes duration.
Other disorders can trigger these or they can occur spontaneously (panic disorder).

39
Q

Which nervous system is involved in anxiety and panic attacks?

A

An excessive fear response leads to the activation of the SYMPATHETIC AUTONOMIC nervous system. Fight-or-flight defence mechanism.

40
Q

Explain pavlovian fear conditioning.

A

Repeatedly presenting a previous neutral conditioned stimulus with an aversive unconditioned stimulus leads to a conditioned fear response.

41
Q

What has Pavlovian fear conditioning been used to study?

A

The acquisition of fears in phobias.

42
Q

Explain the role of the amygdala in fear conditioning.

A

Emotional association and response.
Receives sensory info from cortex, thalamus and hippo.
Sends projection to brain regions involve in emotional responses.
Critical in fear response.
Processes sensory info and passes it onto the central nucleus which in turn activates hypothalamus which activates the SYMPATHETIC AUTONOMIC nervous system.

43
Q

When has the role of the amygdala been demonstrated?

A

Mice studies.
fMRI studies in humans.
Amygdala activated when fearful faces are seen.
Patients with damaged amygdala = lower levels of fear.

44
Q

Explain the role of the hippocampus in fear.

A

Learning the factual information about fear and its context - fear memories.
Patient with hippo damage shows fear response but has no recollection of the fear conditioning.

45
Q

How do the amygdala and hippocampus systems relate to each other?

A

They are independent of each other but interacting for fear learning.

46
Q

How does fear extinction occur?

A

When the feared conditioned stimulus is repeatedly presented by itself.
This exposure leads to an inhibitory memory when suppresses the expression of fear associations.

47
Q

How is the ventromedial prefrontal cortex involved in extinction?

A

It inhibits the memory of the association.

However, EXTINCTION DOES NOT EQUAL FORGETTING.

48
Q

What is some evidence of the vmPFC being involved in extinction?

A

When this area has lesions, extinction is impaired.
Stimulation of this are leads to enhanced inhibition of the conditioned response.
When undergoing extinction training - vmPFC neutrons are activated.
Stronger vmPFC activation = more extinction success (Phelps).

49
Q

What are the main brain characteristics of anxiety disorders?

A

Amygdala over-activation.

PFC under-activation (during emotional regulation tasks).

50
Q

What happens to amygdala and PFC activity after exposure therapy?

A

Amygdala over-activation disappears.

Increases activity in PFC - cognitive control of fear response.

51
Q

How do benzodiazepines work for anxiety disorders?

A

Bind to GABA(little)A receptors which lead to enhanced GABA activity - increased activity at GABA receptor - increased inhibitory tone - sedative effects.
Reduce amygdala activity. Dose-dependent.
Doesn’t effect PFC.

52
Q

What is GABA?

A

An inhibitory neurotransmitter.

Decreases chances of neuron firing action potential.

53
Q

How do SSRIs work for anxiety disorders?

A

Increase serotonin (serotonin system has diffuse modulatory effect on distributed brain activity).
Decrease amygdala activation in both normal and anxious people.
Normalises hippo output under stress conditions.

54
Q

Why do most treatments no longer use benzodiazepines?

A

Dependence concerns.

55
Q

How does exposure to early life stressors and sensitivity to stress affect the hypothalamic pituitary adrenal system?

A

Long-term effect.

Impairs coping mechanisms and induces low tolerance to stress - raises risk of anxiety/mood disorders.

Biological Psychology 2 (11 decks)

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