13. Psychological Disorders

Question 1

Why are psychological disorders so difficult to define?

Answer 1

Because we don’t understand the underlying biological causes. Unlike physical disorders, we can’t match symptoms to exact causes, consequently we can’t find accurate treatments.

Question 2

What is addiction?

Answer 2

A strong and harmful need to regularly have or do something. Can be substance related or activity related. It is compulsive engagement in rewarding stimuli, despite adverse consequences.

Question 3

What do different addictions share in common?

Answer 3

They affect either dopamine or norepinephrine.

Question 4

What are agonists and what are antagonists?

Answer 4

Agonists - drugs that occupy receptors and activate them.

Antagonists - drugs that occupy receptors but do not activate them.

Question 5

What happens if an agonist and antagonist want to bind to the receptor at the same time?

Answer 5

There will be less activation

Question 6

What is drug affinity?

Answer 6

The tendency to bind to a receptor
Different drugs have different affinity
Low affinity –> low tendency to bind to receptor (need higher concentrations of the drug to bind) vice versa

Question 7

What is drug efficacy?

Answer 7

The tendency to activate receptor; level of activation after binding.
More ions can flow through –> higher efficacy

Question 8

Why do people respond differently to drugs?

Answer 8

Different people have different types of receptors. The slight difference does not affect function, but they may affect drug affinity. We have a lot of variability across multiple molecules and proteins. Move towards individualised drugs for specific people.

Question 9

Is a drug with high affinity, and low efficacy an antagonist or agonist?

Answer 9

Antagonist. Even though it binds, but activity is low. Fight for space with neurotransmitters.

Question 10

What are the 3 ways can drugs affect synaptic activity?

Answer 10

1) Affect production of dopamine
2) Interfere with dopamine release
3) Affect how long dopamine is present in the synaptic cleft.

Question 11

What are 2 ways drugs can affect production of dopamine?

Answer 11

1) AMPT blocks the reaction that creates dopamine

2) DOPA can increase the supply of dopamine

Question 12

What are 2 ways drugs can affect release of dopamine?

Answer 12

1) Reserpine make vesicles leaky, causing them to escape from the vesicles
2) Some depressants convert dopamine to an ineffective form of dopamine (DOPAC)

Question 13

What are 2 ways drugs can affect how long dopamine is present in the synaptic cleft?

Answer 13

1) Cocaine blocks reuptake
2) Typical antipsychotic drugs block dopamine receptors by binding to them (antagonist), so dopamine will have less of an effect.

Question 14

What is the main brain structure involved in addiction?

Answer 14

Nucleus accumbens

Question 15

Describe how the nucleus accumbens is involved in addiction?

Answer 15

Nucleus acccumbens is located in ventrial striatum of basal ganglia
Receives input from dopaminergic nucleus.
Ventral tegmental area (VTA) releases dopamine and projects to nucleus accumbens (and other parts of limbic system like amygdala, medial prefrontal cortex involved in reward processing.)

Question 16

What do abused drugs tend to do with synaptic activity?

Answer 16

Increase the activity of dopamine and norepinephrine in the synapse.

Question 17

How does nicotine affect dopamine transmission?

Answer 17

Increase amount of dopamine released from VTA to nucleus accumbens. So nucleus accumbens activates more strongly in response to drug consumption. (and other pleasurable experiences)

Question 18

How does repeated exposure to addictive substances change your brain structure? (3)

Answer 18

1) increase number of receptors in nucleus accumbens
2) increase receptor sensitivity (allow drugs to bind more easily)
3) Increase in metabolism of substance in bloodstream.

Question 19

What do the changes in brain structure result in?

Answer 19

Drug tolerance
- require a higher dose of drug to achieve same effect
Withdrawal
- refers to symptoms that occur after drug cessation
- symptoms include shaking, vomiting, hallucinations, fatigue, convulsions

Question 20

What method is used to examine risk factors of a disorder in a population?

Answer 20

Prospective cohort study.

• See the probability of two groups (alcoholic vs non alcoholic fathers) developing alcoholism.
• Follow up for many years
• If higher probability in one group, could be genetic or upbringing factors
• If same probability, likely just environmental influences

Question 21

What are the possible environmental factors identified to be involved in adddiction?

Answer 21

• prenatal and childhood environment

Question 22

What are depressive disorders?

Answer 22

Refers to a group of disorders characterized by the presence of sad, empty, or irritable mood which significantly affect the individual’s function.

Question 23

What are the possible genetic factors for people with early onset depression?

Answer 23

• more likely to have relatives with depression

Implies either genetic or early upbringing developmental effect transmitted through problems

Question 24

What are the possible genetic factors involved for people with late-onset depression?

Answer 24

• linked to relatives with circulatory problems

possibly due to neurodegeneration of nucleus accumbens

Question 25

Describe a possible genetic-environmental interaction in development of depression.

Answer 25

Serotonin transporter gene Stressful life events those with ss gene more likely to develop depression with increasing number of stressful life events. those with ll gene less likely. regardless of no. of stressful life events, probability remains low

Question 26

What do antidepressants tend to do?

Answer 26

tend to alter serotonin and/or norepinephrine neurotransmission. Serotonin/Norepinephrine reuptake inhibitors Serotnonin (only) reuptake inhibitors more popular

Question 27

Why is it that the prolonged presence of serotonin/norepinephrine in the synaptic cleft is not the likely mechanism for antidepressants?

Answer 27

Because this logic means that serotonin levels go up within minutes or hours, and will stay increased for a long time. But antidepressants take weeks or even months to exert their therapeutic effects. Possible that there are long term changes expressed through genes but mechanism is still unclear.

Question 28

Are antidepressants effective?

Answer 28

Depends on the severity. Low severity -- taking drug or placebo will likely see similar effects High severity -- drug is significantly more effective than placebo.

Question 29

What are alternatives to antidepressants?

Answer 29

1) cognitive behavioural therapy (CBT) 2) exercise 3) electroconvulsive therapy

Question 30

What are some treatments to depression that are under development?

Answer 30

1) Trancranial Magnetic Stimulation (TMS) 2) Deep Brain Stimulation (DBS) 3) Vagal nerve stimulation (VNS)

Question 31

What is an evidence to show that antidepressants don't directly improve mood?

Answer 31

antidepressants increase levels of neurotransmitters very fast, but improvements in mood may take weeks

Question 32

Psychotherapy is preferable to drugs because: (2)

Answer 32

1) produces no side-effects | 2) lower likelihood of relapse after the therapy

Question 33

What are some characteristics of schizophrenia?

Answer 33

- hallucinations - disorganised speech - disorganised behaviour - delusions (unjustifiable beliefs) - weak or absent signs of emotion, speech, and socialisation

Question 34

What are positive symptoms and negative symptoms?

Answer 34

Positive - behaviours that are present but should not be there Negative - behaviours that are absent but should be there

Question 35

What is hypothesized reason for disorganised thought?

Answer 35

Due to a dysfunction of working memory due to abnormal connections between cortex, thalamus, and cerebellum. Working memory and attention are core cognitive functions, when they are taxed sufficiently, can generate incoherent schizophrenic speech.

Question 36

For kids with a genetic predisposition to schizophrenia, what is an important environmental factor that determines if they will actually develop schizophrenia?

Answer 36

Family dysfunction

Question 37

At this point of research, what is the most likely mechanism of schizophrenia?

Answer 37

New mutations (rather than inheriting mutated genes from parents) is the most likely mechanism. Mutations are happening all the time at a slow rate. Random mutations can cause development of Scizophrenia.

Question 38

How does the neurodevelopmental hypothesis explain the development of schizophrenia?

Answer 38

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

Question 39

Which factors elevate the likelihood of schizophrenia?

Answer 39

``` Poor nutrition during pregnancy Stress during pregnancy Head injury during early childhood Infections and injections during pregnancy Owning cats during childhood ```

Question 40

What brain abnormalities do people with schizphrenia have?

Answer 40

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

Question 41

What does the dopamine hypothesis state about development of schizophrenia?

Answer 41

States that dopamine is an important factor in schizophrenia. Dosage of medication needed to see behavioural benefits is almost perfectly correlated with the dosage necessary to block dopamine receptors. Drugs that block dopamine receptors work as an antipsychotic.

Question 42

What does the Glutamate hypothesis state about the development of schizophrenina?

Answer 42

States that drugs that block dopamine synapses indirectly affect glutamate activity. During LTP, Schizophrenia is associated with less release of glutamate and less numbers of NMDA receptors.

Question 43

How does the drug PCP ("angels dust") induce symptoms of schizophrenia?

Answer 43

PCP (“angels dust”) is a drug that inhibits NMDA receptors, specific NMDA blocker. It induces many of the positive and negative symptoms of schizophrenia, without affecting dopamine.