Chapter 13 - Psychological Disorders Flashcards

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1
Q

What is a mental disorder, according to the DSM-5?

A

A syndrome characterized by clinically significant disturbance in an individual’s cognition, emotion regulation or behaviour that reflects a dysfunction in the psychological, biological or developmental processes underlying mental functioning.

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2
Q

What does the word “syndrome” say about mental disorders? (2)

A

A group of symptoms that consistently occur together, assuming they have some common cause?

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3
Q

What does the term “clinically significant” mean?

A

The disorder must create a “serious” problem in your life and the lives of others.

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4
Q

What does it mean to bring “cognition, emotion regulation and behavior” into mental disorder?

A

These 3 factors are all interlinked. There will always be some physical or biological substrate to explain changes in behavior.

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5
Q

Does the DSM-5 define expectable or culturally approved responses to common stressors or loss?

A

No, hence making this vague and ambiguous. That said, some are rather universal. Eg: Someone dies and a person feels very sad –> this is normal.

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6
Q

Is socially deviant behaviour (eg politics, sexual or religious) and conflicts that are primarily between the individual and society mental disorders? Are there any exceptions?

A

No, unless the deviance/conflict results from a dysfunction in the individual.

Eg: Just bc someone is LGBT/communist doesn’t mean they have a mental disorder.

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7
Q

Why is it so difficult to define what a mental disorder is?

A

Because we don’t understand the underlying biological causes. Notice that socio-cultural factors also affect the biology of the organism, but eventually, the issue lies within your physical body.

Unlike physical diseases, we don’t have this level of understanding with mental disorders. We cannot match symptoms to exact causes, and consequently find accurate treatments.

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8
Q

List 2 types of addictive disorders.

A

Substance-related: Drugs, alcohol, cigarettes

Activity: Gambling, work, food

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9
Q

Define what addictive disorders are and one similarity between the 2 types of addictive disorders.

A

Compulsive engagement in rewarding stimuli, despite adverse consequences.

They affect either dopamine or norepinephrine.

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10
Q

Describe three ways substances can interact with receptors.

A

Agonist: Drugs that occupy receptors and activate them
Antagonist: Drugs that occupy receptors but don’t activate them.

Agonist alone binds to receptor: Full activation of the cell
Agonist + Antagonist: Since both reach at the same time, there is less activation of the cell.
Antagonist: No activation.

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11
Q

What is drug affinity?

A

The tendency to bind to receptor
Different drugs have different affinity
- Low affinity means there is a low tendency to bind to receptor (not easy to bind). So you need high concentrations of the drug.
- High affinity: Low concentration may be enough to activate full potential.

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12
Q

What is drug efficacy?

A

The tendency to activate receptor.

Once molecules are bound to receptor, the more ions flow through, hence the higher the efficacy.

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13
Q

What is drug effects variability?

A

Different people have different types of receptors. Hence, different people will respond differently to drugs. We have many proteins encoded in our genome. Whatever subset of our proteins susceptible to binding to drugs.

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14
Q

What can drug effects variability affect?

A

Drug affinity.

We have a lot of variability across multiple molecules. Some drugs may have different effects on people.

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15
Q

List briefly 3 ways drugs can influence synaptic activity.

A

1) Some drugs affect the production of DA (dopamine)
2) Some drugs interfere with DA release.
3) Some drugs affect how long DA is present in the synaptic cleft.

Production, release, duration of presence in synaptic cleft.

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16
Q

How do drugs affect the production of dopamine?

A

AMPT can block the reaction that creates DA. DOPA can increase supply of dopamine.

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17
Q

How do drugs interfere with DA release (2) ?

A
  1. Eg: Reserpine makes vesicles leaky so dopamine escapes from the vesicle.
  2. Eg: Certain anti-depressants converts dopamine into an ineffective form of dopamine (DOPAC) –> Blocks original reaction.
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18
Q

How do drugs affect how long DA is present in the synaptic cleft?

A

Eg: Cocaine blocks reuptake. Typical antipsychotic drug blocks receptor (antagonist) so dopamine has less effect.

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19
Q

Which is the main brain structure involved in addictive disorders? What does it release?

A

Nucleus accumbens

Dopamine and norepinephrine

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20
Q

Nucleus accumbens is part of the _____________ in basal ganglia.

A

Ventral striatum

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21
Q

Describe the projection of dopamine to the ventral striatum.

A
  1. Ventral tegmental area (VTA) releases dopamine and projects to ventral striatum.
  2. Dopaminergic nucleus projects to nucleus accumbens, amygdala and medial prefrontal cortex. All of these are thought to be part of the limbic system - related to reward processing.
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22
Q

List 3 other stimuli that the nucleus accumbens respond to. What does this say about this brain part?

A

Sexual excitement, music, taste of sugar

It helps us process what is good and what we like in our daily lives.

23
Q

List 3 ways repeated exposure to addictive substances can change one’s brain.

A

1) Increase the number of receptors in nucleus accumbens
- Evidence: Rats addicted to cocaine have higher concentration of opiate receptors in nucleus accumbens. Suggests that consumption of drugs changes brain structure.
2) Increase in receptor sensitivity –> Allow drugs to more easily bind to receptors. Change in gene expression results in this.
3) Increase in metabolism of substance in bloodstream (Ie alcohol) changes how you metabolize the substance.

24
Q

List 2 consequences of repeated exposure to addictive substances.

A
  1. Drug tolerance.
    As addiction develops, the effects of the drug decrease, thus requiring a higher dose to achieve the same effect.
  2. Withdrawal.
    Symptoms that occur after cessation - shaking, vomiting, fatigue, hallucinations and convulsions. Can be quite stressful for drug addicts to go into withdrawal.
25
Q

Describe how prospective cohort studies can be used to study risk factors in addictive disorders.

A

1) See how their physiology and behavior change in response to alcohol: must do follow-up for many years
2) See the probability of 2 groups developing alcoholism - higher probability means genetic/upbringing factors, same means environmental factors.

26
Q

List 2 environmental risk factors for substance-related risk factors.

A

Prenatal and childhood environment

27
Q

What are depressive disorders?

A

A group of disorders characterized by the presence of sad, empty or irritable mood which significantly affects the individual’s function.

  • Person feels sad and helpless most of the day every day for long periods of time
  • Person does not enjoy anything and cannot imagine enjoying anything (not even happiness and joy)
  • Fatigue, feelings of worthlessness or contemplation of suicide.
  • Trouble sleeping and concentrating
  • Some people suffer long-term depression but it is more common to have periodic episodes of depression.
28
Q

Describe how genes and environment can interact to produce a certain probability of developing depression.

A

Genes: Serotonin transporter gene (homo recessive = most at risk)

  • Some people are immune to depression, no matter how many stressful life events they have in their lives.
  • However, hormonal changes after birth can lead to temporary episodes of depression.
  • If one does not experience any stressful life event, they won’t get depression. It doesn’t matter what form of serotonin transporter gene you have.
  • If a person experienced many stressful life events, the short form of the serotonin transporter gene will lead to a major increase in probability of developing depression
29
Q

Describe the genetic risk factors of depression

A

People with early-onset depression (before age 30) are more likely to have relatives with depression. Implies either genetics or early upbringing development effect transmitted through problems

People with late-onset depression (after 45) linked to relatives with circulatory problems. Possible neurodegeneration of accumbens neurons –> developing of symptoms if degen sufficient amount.

30
Q

Most common antidepressants alter _____ and/or _________ neurotransmission.

A

Serotonin and norepinephrine

31
Q

List 2 examples of serotonin/norepinephrine reuptake inhibitors.

A

Duloxetine and venlafaxine

32
Q

List 5 examples of serotonin reuptake inhibitors.

A

Fluoxetine, sertraline, fluvoxamine, citalopram and paroxetine.

33
Q

By inhibiting reuptake of serotonin, what happens?

Why is this mechanism not the reason why antidepressants work?

A

Prolonged presence of neurotransmitter in synaptic cleft

Because this logic means that serotonin levels will go up within minutes or hours and will stay increased for along time. But antidepressants take weeks or even months to exert their therapeutic effects. Hence, increased serotonin levels may not be the key reason why antidepressants work. Might be possible that there are long-term changes expressed through genes but mechanism is still unclear.

34
Q

Describe the difference in the effectiveness of antidepressants between low-severity and high-severity cases.

A

Low severity: Doesn’t matter whether drug or placebo is used. Improvement in condition is the same.

High severity: Significant difference between placebo and drug. Drug very effective in driving improvement.

Highlights that you cannot just give a drug to anyone who comes in. Must assess the severity to see if other forms of therapy are better.

35
Q

What is a good alternative to drugs for cases with low-severity?

A

CBT. no side effects and lower chances of relapse also

36
Q

What is a caveat about deep brain stimulation?

A

Electrodes put in brain –> Patients do see better outcomes but they have to pay large amounts of money if they don’t want it removed. Insurance don’t cover

37
Q

What is schizophrenia and what are its symptoms?

A

Deteriorating ability to function in everyday life for at least 6 months, paired with at least 2 of the following symptoms, including at least 1 of the first 3

  • Hallucinations: hearing voices
  • Delusions: unjustifiable beliefs
  • Disorganized speech
  • Grossly disorganized behaviour
  • Weak or absent signs of emotions
38
Q

___________ symptoms are behaviours that are present, but should be absent.

A

Positive

39
Q

Negative symptoms are ________________.

A

Behaviours that are absent but should be present.

40
Q

What is hypothesized about the cause of schizophrenia?

A

Since disorganized thought is the core of schizophrenia, it could be that dysfunctional working memory causes it. This, in turn, is due to abnormal connections between the cortex, thalamus and cerebellum.

41
Q

List 2 areas that show dysfunction in schizophrenic patients and provide evidence.

A

Attention and working memory.

Do 2 tasks at one go. Show them pictures and ask them to come up with a story. Avoid what they said first time and tell a different story. The memory task causes even greater interference and their speech become incoherent –> schizophrenic speech.

42
Q

Provide evidence about how genes and environment appear to play equal parts in creating the probability for schizophrenia.

A

For kids with genetic risk to schizo, family dysfunction will be important in determining likelihood of developing it. Family risk is less risk than upbringing.

43
Q

What does the contribution of environmental risk factors to schizo say about it?

A

Likely mechanism: new mutations, rather than inheriting mutated genes.

44
Q

What does the neurodevelopmental hypothesis propose about schizophrenia?

A

States that an important factor in the development of schizophrenia is a disturbance in development (in-utero or early childhood)

45
Q

List 4 examples of how in-utero and early childhood disturbances can increase risk of schizo.

A

1) Poor nutrition during pregnancy
2) Stress during pregnancy
3) Head injury during early childhood
4) Infections and fever during pregnancy

46
Q

What are some anatomical abnormalities observed in schizo patients?

A

While most results are inconsistent, but:

  • Smaller left prefrontal and temporal cortices
  • Small cell bodies in hippocampus and prefrontal cortex: may be related to failures in connectivity
  • More dominant right hemisphere
47
Q

What is the dopamine hypothesis?

A

States that dopamine is an important factor in schizophrenia. Dosage that patients needed to take daily to see behavioural benefits is almost perfectly correlated with dosage necessary to block dopamine receptors.

Drugs that block dopamine synapses work as antipsychotic. Increases dopamine release during 1st psychotic episodes.

48
Q

What is substance-induced psychotic disorder?

A

Has similar symptoms as schizo. But induced by drugs such as cocaine, which increases dopamine in synapses.

49
Q

What is the glutamate hypothesis?

A

Deficient activity of glutamate synapses in the prefrontal cortex.

Drugs that block dopamine synapses also affect glutamate activity indirectly.
Schizophrenia is associated with less release of Glu and less numbers of NMDA receptors.

RECALL LTP AND NMDA RECEPTORS

50
Q

What drug inhibits NMDA receptors and induces symptoms of schizo?

A

PCP

51
Q

List 5 characteristics of ASD.

A
  1. Deficits in social and emotional exchange.
  2. Deficits in gestures, facial expressions and other nonverbal communication
  3. Stereotyped behaviors like repetitive movements
  4. Resistance to a change in routine
  5. Unusually weak or strong responses to stimuli, such as indifference to pain or a panicked reaction to a sound
52
Q

List the genetic risk factors of ASD.

A

New mutations, and not mutations inherited from parents.

53
Q

List the environmental risk factors of ASD.

A

Prenatal environment

12% of mothers of autistic children have antibodies that attack certain brain proteins (almost 0% in for mothers of non-autistic children)

High intake of folic acid reduces risk of autism by half