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Brain, Biology and Behaviour > Week 10 - mental disorders > Flashcards

Week 10 - mental disorders Flashcards

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1
Q

Symptoms for major depression

A
  1. Sad mood
  2. Loss of interest and pleasure
  3. Difficulties sleeping/excessive
  4. Shift in activity level - lethargic/agitated
  5. Poor appetite+weight loss/opposite
  6. Loss of energy
  7. Negative self-concept
  8. Difficulty in concentration
  9. Recurrent thoughts of death or suicide
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2
Q

Monoamines involved in depression (Monoamine hypothesis for depression) -

A

Serotonin + Norepinephrine

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3
Q

Which factors of depression can be explained by low level monoamines?

A

reduction in sleep, appetite, sex, motor activity.

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4
Q

Why are monoamines so affecting for these factors?

A

The hypothalamus controls sleep, appetite, sex and motor activity.

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5
Q

How do Tricyclics and SSRI’s work?

A

Prevent reuptake/reabsorption of seretonin and norepinephrine by presynaptic neuron. Fit into channels through which monoamines would be reabsorbed.

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6
Q

What does “tricyclic” refer to?

A

The chemical structure of the drug.

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7
Q

What are bicyclics?

A

SSRI’s.

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8
Q

Do most SSRI’s have fewer side effects than tricyclics?

A

Yes!

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9
Q

What do MAOI inhibitors do?

A

Inhibits the breakdown of neurotransmitter in the synapse.

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10
Q

What is the worst side effect of MAOIs?

A

Fatally high blood pressure when taken in combination with certain foods that contain tyramine (cheese, aged meats, wines, some beers, stimulants, tricyclics).

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11
Q

How many volts and for how long does ECT use?

A

70-150 volts for 0.1 - 1 second. Convulsion runs course for 45-60 seconds.

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12
Q

How effective is ECT?

A

About 70% of severely depressed patients.

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13
Q

How many people die from ECT?

A

1/1000.

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14
Q

What are other side effects?

A

Headaches and memory loss.

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15
Q

What results in too much monoamine neurotransmitter?

A

Mania.

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16
Q

What is the dysregulation hypothesis?

A

The amounts of neurotransmitters are either too high or too low due to poor regulation.

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17
Q

How does lithium work for bipolar?

A

Works by moderating the level of norepinephrine.

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18
Q

What are side effects of lithium?

A

Problems with concentration, thirst, poor motor coordination, mucsle tremors and dizziness.

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19
Q

What do you need to do while taking lithium?

A

constantly monitor blood levels are high amounts are blood are poisonous.

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20
Q

What are the positive symptoms of schizophrenia?

A
  • Delusions or unfounded beliefs
  • auditory hallucinations
  • thought disorders (eg. difficulty understanding and using abstract concepts)
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21
Q

What are the negative symptoms of schizophrenia?

A
  • Poverty of speech (incoherent thoughts)
  • Limited emotional expression
  • Anedonia - inability to experience pleasure
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22
Q

Common delusion of schizophrenia?

A

Delusion of persecution - thinking someone is spying on them and wants to hurt them.

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23
Q

What is the neurodevelopmental hypothesis of schizophrenia?

A

Genes plus abnormalities during the prenatal or neonatal periods impair brain development and lead to schizophrenia.

24
Q

What evidence is there for the neruodevelopmental hypothesis for schizophrenia?

A

Linked with poor nutrition in pregnancy, premature birth or low birth weight, delivery complications.
-people born in winter have 5-8% higher rate (possibly due to increased viral infection rates for mother)

25
Q

What causes larger ventricles?

A

Infection during fetal development.

26
Q

What other neurological differences in schizophrenia?

A

Cell bodies are smaller in limbic system (hippocampus, amygdala and basal ganglia), and prefrontal cortex.

27
Q

What is the dopamine hypothesis of schizophrenia?

A

Excess dopamine activity causes behavioural changes associated with schizophrenia - positive symptoms (halucinations etc.)

28
Q

What 3 sets of evidence for dopamine hypothesis?

A
  1. Drugs that act on dopamine reduce positive symptoms of schizophrenia.
  2. Drugs increasing dopamine (cocaine) increase schizophrenic symptoms.
  3. People with schizophrenia have more dopamine receptors than normal.
29
Q

Glutamate hypothesis?

A

Schizophrenia caused by low glutamate activity, especially in pre-frontal cortex.

30
Q

What does dopamine inhibit?

A

Glutamate release.

31
Q

So what would increased dopamine cause?

A

Decreased glutamate.

32
Q

What happens if you’ve got low serotonin, regarding dopamine?

A

Dopamine will be less inhibited.

33
Q

What is schizophrenia treated with?

A

Antipsychotics (neuroleptics) - block dopamine receptors

34
Q

Which symptoms are treated with neuroleptics?

A

Positive.

35
Q

What are the side effects of the common neuroleptics?

A

Tardive dyskinesia - tremours, involuntary movements

36
Q

What are the newer neuroleptics?

A

Atypical neuroleptics/antipsychotics.

37
Q

What’s the difference with atypical neuroleptics?

A

They also increase serotonin, which inhibits dopamine activity.

38
Q

Why are they called atypical neuroleptics

A
  1. They block fewer dopamine receptors than regular neuroleptics.
  2. More sensitive to which receptors are blocked (block tracks that lead to frontal and temporal lobes, but not associated with motor movements) - reducing motor side effects
  3. Influence serotonin activity - reduce dopamine levels.
39
Q

What are the limitations to drug therapy for schizophrenia

A
  1. Treatment, not cure.
  2. Drugs are effective for treating POSITIVE symptoms.
  3. Not all patients are not helped by drugs.
  4. Side effects
40
Q

How do benzodiazepines work?

A

They facilitate transmission of Gamma-aminobutyric acid (GABA)
Binds to GABA receptors and laters the shape of receptors so that GABA ATTACHES MORE EASILY and BINDS more tightly.

41
Q

Which brain areas are effected by benzos?

A

Amygdala and hypothalamus - increased GABA - suppress/reduce arousal.

42
Q

What are benzo side effects?

A

Drowsiness, nausea, constipation, physical dependency.

43
Q

What is a more reliable symptom for major depression than increased sadness?

A

Lack of happiness.

44
Q

Which part of the brain becomes less sensitive to reward when a patient is depressed?

A

The Nucleus Accumbens.

45
Q

Is impaired sense of smell a symptom of depression?

A

Yes!

46
Q

Which symptoms often persist after the MOOD symptoms of depression are treated?

A

The cognitive symptoms.

47
Q

What is the prevalence of major depression?

A

Around 5-6% during any given year, and 10% across lifetime.

48
Q

What is more common? Long-term depression or episodic depressioN?

A

Episodic.

49
Q

To what degree of heritability does depression have?

A

Moderate.

50
Q

What role might the immune system have on depression?

A

Increased activity of the immune system (from poor diet, highly stressful situations, injury etc.) can negatively affect depression.

51
Q

What is the effect of a short form vs. a long form of the gene that controls the serotonin transporter?

A

Two short forms = increases likelihood of depression from stressful events
Two long forms = decreased likelihood of depression from stressful events

52
Q

Is this gene solely responsible for depression?

A

The short form INCREASES EMOTIONAL REACTIVITY. So, no. It is also responsible for smiles, laughter, or anger depending on the event.

53
Q

Which hemisphere is associated with depression and with what activity?

A

Reduced activity of the left hemisphere is associated with depression, increased activity in the right pre-frontal cortex.

54
Q

Which part of the brain is larger in people with Bipolar Disorder?

A

The amygdala (important for emotions).

55
Q

Which brain part is smaller in people with PTSD?

A

the hippocampus.

56
Q

Does PTSD cause small hippocampus, or does the hippocampus (plus trauma) cause PTSD?

A

Who knows.

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