Psychiatric Disorders, Drug Action and Addiction Flashcards

(45 cards)

1
Q

How do drugs function?

A

They tend to imitate substances already present in our nervous system, especially those that affect transmission at the synapse

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2
Q

Legal drugs

A

nicotine, alcohol, caffeine

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3
Q

illegal drugs

A

cocaine, opiates, LSD

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4
Q

Why do plants make drugs?

A

The plant produces chemicals to attract insects and to stop being eaten - our nervous systems are very similar to animals

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5
Q

How do drugs work?

A

Drugs can affect transmission at the synapse in two ways: antagonist and agonist . Antagonists block the neurotransmitter, agonists increase the effects of neurotransmitters, or mimic the neurotransmitter. Some drugs can do both depending on the dose.

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6
Q

When does a drug have a high affinity for a receptor?

A

If it binds to the receptor but may not activate the receptor

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7
Q

When does a drug have a high efficacy for a receptor?

A

If it has a tendency to activate that receptor

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8
Q

What do most drugs stimulate the release of?

A

The release of dopamine particularly in the nucleus accumbens (a small subcortical area rich in dopamine receptors) a part of the dopamine pathway

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9
Q

Describe the pathway of dopamine after a drug has been taken

A

Drug => Sustained bursgs of dopamine (usually inhibitory) => inhibits GABA (inhibitory transmitter) => increases activity in nucleus accumbent

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10
Q

What are stimulants - how do they work?

A

Amphetamine - stimulates dopamine synapses by increasing the release of dopamine from presynaptic terminal

Cocaine - blocks the reuptake of dopamine, thus prolonging effects

These are dopamine agonists and cause an accumulation of dopamine in the synaptic cleft

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11
Q

What does it mean if there is more dopamine?

A

Widespread reduction in activity in most of the brain (apart from nucleus accumbens)

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12
Q

What are opiates - how do they work?

A

Morphine and heroin increases relaxation and decreases sensitivity to pain due to mimicking endorphins . They attach to specific endorphin receptors which inhibits GABA to increase dopamine BUT opiates also block a hindbrain area that usually releases norepinephrine. A reduction in norepinephrine reduces memory storage and reduces stress.

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13
Q

Why are dopamine highs followed by a crash?

A

Dopamine washes away and can’t be replaced quick enough

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14
Q

What is Marijuana - how do they work?

A

Contains cannabinoids which bind to specific cannabinoid receptors which are widespread in the brain. Cannabinoids inhibits GABA release which increases perception of heightened awareness. Cannabinoid receptors are abundant in the hypothalamus which is related to feeding so we have an increased appetite.

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15
Q

What is Botox - how do they work?

A

Botilinium toxins are usually found in decaying food but small doses are used to block the release of acetylcholine at neuromuscular junctions (paralysis) to reduce tremors and for cosmetic purposes.

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16
Q

Is there a difference between wanting and liking?

A

Drugs increase ‘need’ for the substance even if the experience is not pleasant. Mice with increased dopamine production showed no more pleasure in food but made more effort to get it. Mice with decreased dopamine production made less effort to get food, but ate just as much.

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17
Q

How does the nucleus accumbens become more sensitised?

A

Becomes more sensitised to substances after repeated use. Increased ability to release dopamine in response to the substance which reduces sensitivity to other things

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18
Q

Explain withdrawal

A

Cravings for the drug , relapse causes increased sensitivity and the user learns that the drug relieves distress associated with withdrawal and so craves it more during future withdrawal.

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19
Q

How can we counter addiction?

A

Varenicline is a drug that acts as a partial nicotine receptor agonist. It binds and stimulates nicotine receptors. It has a very high affinity which means that are nicotine finds it very difficult to bind onto the receptor. So you get the effect of nicotine but if you then smoke you don’t get much more of a dopamine reward.

20
Q

What is the most common drug addiction ?

21
Q

Define drug addiction

A

Continued use of a substance which interferes with your life

22
Q

What effect does alcohol have?

A

Inhibitory effects that relax the brain and communication - stimulates GABA activity and increases dopamine

23
Q

What is type 1 alcoholism?

A

Late onset (after 25), gradual onset, equal men and women and is less severe. Fewer relatives with alcoholism

24
Q

What is type 2 alcoholism?

A

Early onset (before 25), rapid onset, more men than women, severe and has more relatives with alcoholism.

25
How might genes influence alcoholism?
1. coding for an increase in risk taking behaviour 2. coding for an increased stress response = more likely to relapse after quitting
26
Do sons of alcoholic fathers show predispositions to alcoholism?
1. Show less than average intoxication - tolerance to alcohol 2. Show greater decrease of stress when drinking 3. Slightly smaller amygdala so maybe increased risk taking
27
How prevalent is depression?
Twice as common in women than men , 5% adults have clinically significant depression
28
Depression symptoms
Feelings of extreme sadness and helplessness, severe enough to interfere with daily life , and can last for weeks or months , feelings of absent happiness
29
What causes depression?
There is a moderate degree of heritability to depression - but this is not specific to depression , relatives are more likely to suffer from anxiety, substance abuse, bulimia etc. Depression is more common along relatives of women with early onset of depression (before 30)
30
Describe serotonin's role in depression
Low serotonin turnover associated with aggression and depression . So genes controlling serotonin have been implicated. In 2003, a particular gene that controlled the transportation of serotonin protein was discovered. There is a short version or a long version of the gene. If you have two short forms of the gene you are more likely to have depression in response to stressful events.
31
What is postnatal depression? How prevalent is it ?
Depression after giving birth. 20% of women experience it but only 0.1% have long lasting. Evidence suggests that it runs in families but it also seems to be universal - perhaps a normal reaction to childbirth.
32
What is unipolar disorder?
Varying between normality and depression
33
What is bipolar disorder?
Varying between mania and depression
34
What is SAD and some symptoms?
Seasonal Affective Disorder - Depression associated with one season . it is common near the poles where the nights are long and is less severe than major depression. Light therapy is used as treatment
35
How do lithium salts treat bipolar?
The salts block the synthesis of arachinodonic acid which is associated with brain inflammation.
36
What is schizophrenia ?
There is a division of emotional and intellectual experiences and behaviour. Some patients show inappropriate emotional expression that seems detached from current circumstances. Other symptoms include hallucinations, delusions and movement disorder.
37
negative symptoms of SZ (absences)
poor social interaction , poor speech, absent facial expression
38
positive symptoms of SZ (additions)
psychotic = delusions , hallucinations disorganised = odd emotional displays , thought disorder
39
What is an issue with schizophrenia diagnosis
Not all patients exhibit all symptoms , difficult to pinpoint a specific brain area. But PET scans have found activation in thalamus , hippocampus and auditory cortex during hallucinations
40
What demographics are affected by sz?
More common in men Earlier onset in men Present in 1% of the population Equal proportions in all cultures/ populations
41
What is the neurodevelopmental hypothesis of SZ?
abnormalities in the development of the nervous system before birth and in the newborn . Could be caused by infections, poor nutrition or a complicated delivery. Could also be due to some slight brain abnormalities in parents.
42
List brain abnormalities associated with schizophrenia
1. larger ventricles so less space for brain cells 2. Damaged prefrontal cortex (working memory) 3. Cell bodies are smaller in the hippocampus and prefrontal cortex (memory consolidation and working memory) 4. Less lateralisation than most people
43
What is the dopamine hypothesis of sz
Excess activity of dopamine synapses - sz patients have twice as many dopamine receptors than other people however normals levels of dopamines are found when measured directly.
44
What is the glutamate hypothesis of sz?
Deficient activity at glutamate synapses
45