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Biological Psychology with Research Methods > Anxiety Disorders and Schizophrenia > Flashcards

Anxiety Disorders and Schizophrenia Flashcards

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1
Q

What is the biopsychosocial approach?

A

Our biology, psychology, and social context interact in order to create a disease.

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2
Q

What contributes to our biology that can affect our health?

A
  • Gender
  • Physical illness
  • Disability
  • Genetic vulnerability
  • Immune function
  • Neurochemistry
  • Stress reactivity
  • Medication effects
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3
Q

What contributes to our psychology that affects our health?

A
  • Learning/memory
  • Attitudes/beliefs
  • Personality
  • Behaviours
  • Emotions
  • Coping Skills
  • Past Trauma
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4
Q

What contributes to our social context that affects health?

A
  • Social Supports
  • Family background
  • Cultural traditions
  • Socioeconomic Status
  • Education
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5
Q

What is the lifetime prevalence of schizophrenia?

A

1%

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6
Q

When is schizophrenia most likely to manifest?

A

Late teens to early 20s

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7
Q

What and when was schizophrenia first described as?

A

1893 - Dementia Praecox

Later was defined as schizophrenia in 1908.

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8
Q

What are positive symptoms of schizophrenia?

A

Involve the presence of symptoms:

  • Delusions
  • Hallucinations
  • Disorganised speech (jumping between topics or nonsense sentences)
  • Grossly disorganised or catatonic behaviour such as rocking
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9
Q

What are negative symptoms of schizophrenia?

A

Involve the absence of response:

  • Reduced expression of emotion (show no interest in anything)
  • Poverty of speech
  • Difficulty initiating goal directed behaviour
  • Neglect of personal hygiene
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10
Q

What is a psychotic episode?

A

A period of intense positive symptoms

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11
Q

What are some examples of cognitive symptoms?

A
  • Poor ability to maintain attention
  • Impaired verbal working memory
  • Inflexible thinking style - difficulty in adapting
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12
Q

What is the difference between the presence of positive/negative symptoms vs cognitive symptoms?

A

Positive and negative symptoms improve and worsen in cycles of relapse and remission, whereas cognitive symptoms are relatively stable over the course of the illness.

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13
Q

What is the DSM-V criteria for schizophrenia?

A

Two or more of the following symptoms must be present for at least 1 month and one of which must be one of the first 3 listed:

  1. Delusions
  2. Hallucinations
  3. Disorganised Speech
  4. Disorganised or catatonic behaviour
  5. Negative symptoms

Also, social/occupational dysfunction and continuous signs of illness for at least 6 months with at least 1 month of active symptoms.

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14
Q

What disorders often have similar symptoms to schizophrenia?

A
  • Mood disorders such as depression or bipolar with psychotic features
  • Substance abuse eg. cocaine or LSD
  • Brain damage
  • Huntingtons, parkinsons, alzheimers
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15
Q

What are the causes of schizophrenia?

A

Often an interaction between genes and the environment but specifically:

  • Genetics
  • Neurodevelopment
  • Brain abnormalities
  • Neurotransmitters
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16
Q

What is the relationship between genetics and schizophrenia?

A

There is evidence for schizophrenia to be based down with genetics. For example, someone whose parent is schizophrenic is 13 times more likely to develop the disease and someone with an identical twin with schizophrenia has a 48% chance of developing it. However, it is not always the case as 85% of those with schizophrenia have no first degree relative with the illness.

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17
Q

Which genes are involved in schizophrenia?

A

A large number of high risk gnes have been identified (more than 100), with some overlapping with other disorders like autism.
Specifically the dopamine receptor (D2) gene - links to treatment but explains less than half of genetic variance.

18
Q

What do gene mutations have to do with schizophrenia?

A

Increased paternal age of conception can lead to gene mutations that lead to increased risk of schizophrenia. Is an explanation for how the lifetime prevalence is still 1% despite the low rates of reproductivity and earlier death rates.

19
Q

What is the gene-environment interaction in schizophrenia?

A

Some genotypes are more likely to develop the disease when exposed to certain environments. Eg. if someone has a parent with schizophrenia and also has a dysfunctional family they are more likely to get the disease.

20
Q

What neurodevleopmental factors can cause schizophrenia?

A
  • Prenatal factors (infections during pregnancy, low birth weight etc) might affect neurodevelopment
  • Cannabis use can increase risk of schizophrenia (unsure of causality however)
21
Q

What brain abnormalities are found in schizophrenia?

A
  • Larger than average ventricles
  • Less grey matter
  • Less white matter (loss of myelin sheath)
  • Less brain connectivity (synaptic over-pruning)
  • Reduced corpus callosum volume

Not sure of cause and effect as these areas worsen during disease.

22
Q

What neurotransmitters are linked to schizophrenia?

A

Dopamine and glutamine systems

23
Q

What is the dopamine hypothesis?

A

Neurones release dopamine faster than average which results in excess activity.

Evidence?

  • Antipsychotic drugs act on dopamine receptors
  • Dopaminergic recreational drugs create symptoms similar to schizophrenia eg. hallucinations in cocaine
24
Q

How do neuroleptic (Typical) drugs work to treat symptoms in schizophrenia?

A

Block D2 receptors which lead to improved positive symptoms (it reduces these symptoms).

Side effects:
More than 80% of binding to d2 receptors can result in extrapyramidal symptoms (eg. rigidity and motor restlessness).

25
Q

What is the difference between typical and Atypical antipsychotics?

A

Typical psychotics work on binding to just D2 receptors and result in side effects related to motor control.

Whereas atypical antipsychotics reduce these risks by working on several receptors (d2,3,4) and serotonin but have other side effects of drowsiness, weight gain and diabetes.

26
Q

What are the limitations of the dopamine hypothesis of schizophrenia?

A
  • 1/3 of patients don’t respond to treatment
  • unclear relationship between dopamine and negative/cognitive symptoms of schizophrenia
  • substance dependence is common which reduces dopamine release
27
Q

What is the glutamate hypothesis of schizophrenia?

A

Schizophrenia is due to NMDA dysfunction (this is a type of glutamate receptor). It seems reduced receptors result in schizophrenia.

Evidence?
NMDA receptor antagonists (eg. ketamine) have positive, negative and cognitive symptoms similar to schizophrenia.
Most explanation we have for negative symptoms

28
Q

What are the limitations of the glutamate hypothesis of schizophrenia?

A
  • Trials have not shown a conclusive strong effect in most cases
  • Close interactions between glutamate and dopamine
29
Q

What is an anxiety disorder?

A

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

30
Q

What is the lifetime prevalence of anxiety disorders?

A

It is estimated that up to 30% of people will suffer from anxiety at one point in their life.

31
Q

What are the most common anxiety disorders recognised by the DSM V?

A
  • Specific phobia (persistent irrational fears of specific objects, activities and behaviours)
  • Social anxiety disorder
  • Generalised anxiety disorder (excessive worry, restlessness, trouble sleeping)
  • Panic disorder (panic attacks)
  • Agoraphobia (anxiety in which the individual perceives their environment to be unsafe
32
Q

What are panic attacks and their symptoms?

A

A feeling of sudden and intense fear and anxiety.

Symptoms:
- rapid irregular heartbeat
- sweating
- trembling
shortness of breath
- chest pain
- nausea
- diziness
- dry mouth
33
Q

What is the biological mechanism behind panic attacks?

A

An abnormal fight or flight defence mechanism.

34
Q

What region of the brain is related to the fear response?

A

Amygdala

35
Q

How does fear conditioning in the amygdala work?

A

Sensory information from the thalamus and cortex are processed in the basolateral nucleus of the amygdala and passed on to the central nucleus. The central nucleus then activates the hypothalamus which in turn activates the sympathetic ANS.

It is related to the emotional association and response to fear and produces a physiological response to fear.

36
Q

How is the hippocampus related to the fear response?

A

It learns the factual information about fear and its context aka. fear memories.

37
Q

What region of the brain is associate with making fear ‘extinct’?

A

The ventromedial prefrontal cortex (vmPFC) - repeatedly presenting a conditioned stimulus (CS) will reduce the conditioned response (CER) as the memory for the association between the two is inhibited by the vmPFC.

38
Q

How is the amygdala involved in anxiety disorders?

A

The amygdala is overactive in anxiety disorders in response to negative stimuli.

39
Q

How is the pre frontal cortex involved in anxiety disorders?

A

This area is under-activated and patients seem less able to use it in emotional regulation tasks.

40
Q

How do benzodizapenes work to reduce anxiety?

A

They bind to GABA receptors allowing an influx of negatively charged ion chlorine which hyperpolarise the neurone, increasing GABA activity which has sedative effects.

Problem:
Drug dependency

41
Q

How do selective serotonin re-uptake inhibitors (SSRIs) treat anxiety?

A

Increase neurogensisis by decreasing amygdala activation and normalise hippocampul output under stress conditions.

42
Q

How is the HPA axis related to anxiety disorders?

A

Exposure to early life stressors and sensitivity to stress impair coping mechanisms and induce low tolerance to stress which raises the risk of anxiety and mood disorders.

Biological Psychology with Research Methods (6 decks)

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