Addiction Flashcards

1
Q

What does addiction mean?

1 - need more of a drug/stimulus to achieve same effects as previously
2 - continue using drug/stimulus despite being aware of the negative consequences
3 - stop taking the drug/stimulus as patient is aware of the negative consequences
4 - normal function of the body is impaired if drug/stimulus is stopped

A

2 - continue using drug/stimulus despite being aware of the negative consequences

  • a compulsive behaviour
  • despite negative effects, patient still gets pleasure/positive reward which provides positive reinforcement and behaviour is reinforcing (compulsion)
  • loss of control in limiting intake
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2
Q

What is Tolerance, also referred to as a hyposensitisation syndrome?

1 - need more of a drug/stimulus to achieve same effects as previously
2 - continue using drug/stimulus despite being aware of the negative consequences
3 - stop taking the drug/stimulus as patient is aware of the negative consequences
4 - normal function of the body is impaired if drug/stimulus is stopped

A

1 - need more of a drug/stimulus to achieve same effects as previously

  • patient does not respond to a substance in the same way, becoming tolerant
  • patient seeks a higher dose or stronger drug for same effect
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3
Q

What is Dependence?

1 - need more of a drug/stimulus to achieve same effects as previously
2 - continue using drug/stimulus despite being aware of the negative consequences
3 - stop taking the drug/stimulus as patient is aware of the negative consequences
4 - normal function of the body is impaired if drug/stimulus is stopped

A

4 - normal function of the body is impaired if drug/stimulus is stopped
- can present with physiological symptoms (alcohol withdrawal)

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4
Q

What is the mesolimbic pathway often referred to as and what is the importance of this?

also referred to as the reward pathway?

1 - known as the reward pathway, a dopaminergic pathway in the brain involved in positive reinforcement
2 - known as the pain sensing pathway, a glutaminergic pathway in the brain involved in positive reinforcement
3 - known as the reward pathway, a sertoninergic pathway in the brain involved in positive reinforcement
4 - known as the emotional pathway, a acetylcholinergis pathway in the brain involved in positive reinforcement

A

1 - known as the reward pathway, a dopaminergic pathway in the brain involved in positive reinforcement

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5
Q

The Mesocorticolimbic pathway is considered to be part of the wider cortico-basal ganglia-thalamo-cortical loop [CBGTC]. What components of the brain make up the CBGTC?

1 - cortex, cerebellum, basal ganglia
2 - cortex, thalamus and brain stem
3 - cortex, brain stem and basal ganglia
4 - cortex, basal ganglia and thalamus

A

4 - cortex, basal ganglia and thalamus

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6
Q

What is the start of the mesolimbic pathway?

1 - ventral tegmental area
2 - substantia niagra
3 - pituitary gland
4 - hypothalamus

A

1 - ventral tegmental area

  • nucleus accumbens (main dopamine nucleus)
  • located in the midbrain
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7
Q

The ventral tegmental area (VTA), located in the midbrain is the start of the mesocorticolimbic pathway. What is the VTA?

A
  • a group of neurons located close to the midline on the floor of the midbrain
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8
Q

The ventral tegmental area (VTA), located in the midbrain is the start of the mesocorticolimbic pathway. The VTA is a group of neurons located close to the midline on the floor of the midbrain. VTA is the start of the mesolimbic pathway, where does it travel to next?

1 - nucleus accumbens
2 - substantia niagra
3 - pituitary gland
4 - hypothalamus

A

1 - nucleus accumbens

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9
Q

What is the cingulate gyrus?

1 - grey matter near centre of the brain involved in relaying information in the brain
2 - located deep in the brain acting as a control coordinating center
3 - primary commissural region of the brain, connecting the left and right cerebral hemispheres.
4 - arch shaped bulge in cerebral cortex involved in regulating behaviour and emotion

A

4 - arch shaped bulge in cerebral cortex involved in regulating behaviour and emotion

  • located above the corpus callosum
  • described as the limbic cortex (involved in emotions and memory), influences emotionally enhanced memories
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10
Q

The ventral tegmental area, nucleus accumbens, prefrontal cortex and the cingulate gyrus are all involved in the mesocorticolimbic pathway. What other 2 key subcortical structures are involved in brain?

1 - amygdala and hippocampus
2 - amygdala and thalamus
3 - brain stem and hippocampus
4 - amygdala and pons

A

1 - amygdala and hippocampus

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11
Q

The image below illustrates the normal pathway for reward and reinforcement based on natural reinforces, such as food and sex. Why is understanding this pathway important for addiction, tolerance and dependance?

1 - often involved in dementia
2 - psychoaddictive subtances can hijack this system
3 - involved in parkinsons disease
4 - often affected on mental health disorders

A

2 - psychoaddictive subtances can hijack this system

  • BUT worse they provide an even greater positive valence than natural rewards (greater positive feeling), meaning they may be more likely to increase the risk of them repeating this regularly
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12
Q

The Nucleus Accumbens (NA), which is part of the mesocorticolimbic pathway is important in processing of cognitive processing of motivation and reward, such as pleasure and re-enforcement. The NA can be stimulated in the anticipation to reward, what is the size of the stimulation of the NA relative to?

1 - the size of the potential reward
2 - the duration of the potential reward
3 - the intensity of the potential reward

A

1 - the size of the potential reward

  • dopamine is released in anticipation of the receiving the reward
  • the bigger the reward the bigger the stimulation required
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13
Q

When we think about the reinforcement system we are aware that there is direct reinforcement from a stimulus, where something good has just occurred and we learn from this experience, and we are more likely to do this again. This is then able to strengthen neural connections between neurons detecting the stimulus and the neurons that produce the instrumental response, called long term potentiation. This is called associative learning (like with the dog, food, bell and saliva). Using cocaine as an example, how does this work?

A
  • patient takes cocaine in a nightclub
  • patient then associated going to a nightclub with taking cocaine
  • clinically important as if someone in remission from cocaine goes to a nightclub they are more likely to relapse
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14
Q

Drug dependance, which is where a patients normal functioning (or at least normal for the patient) is dependent on the drug that they are taking. Drug dependence has been shown to cause homeostatic neuronal adaptations (changes in normal neuronal function due to the stimulus) to the drug. What can this then cause in the brain and result in?

1 - synaptic plasticity (changes in neuronal connections)
2 - associatve learning (reward becomes associated with psychoaddictive substances)
3 - increased autonomic activity (increased with substance, but remains active when substance is stopped)
4 - all of the above

A

4 - all of the above

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15
Q

Long term potentiation is when a synaptic connection is constantly stimulated, For example, NMDA and AMPA glutamate receptors are stimulated. Extended opening of NMDA receptors increases intracellular Ca2+. The increased intracellular Ca2+ signals for the increase of AMPA receptors on the membrane, More receptors on the membrane makes them more sensitive to glutamate and more likely to cause an action potential. Which dopamine receptors are involved in long term potentiation?

1 - D1 receptors
2 - D2 receptors
3 - D3 receptors
4 - D4 receptors

A

1 - D1 receptors

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16
Q

Dopamine D1 receptors are involved in long term potentiation through the modification of glutamatergic transmission, which then allows long term potentiation (essentially more glutaminergic receptors are located on the cells membrane). What does this do to the synapses on dendrite spines and branches?

1 - nothing
2 - dendrite number and length increases
3 - synaptic remodelling causing increased number of dendritic spines
4 - synaptic remodelling causing a decreased number of dendritic spines

A

3 - synaptic remodelling causing increased number of dendritic spines
- more dendritic spines increase the surface area to receive information)

17
Q

Dopamine D1 receptors are involved in long term potentiation in cocaine addiction through the modification of glutamatergic transmission, which then allows long term potentiation. This causes synaptic remodelling (essentially means more dendritic spines that increase surface area to receive information). Even in abstinence do these changes just disappear?

A
  • no
  • dendritic spines can remain for months following abstinence
  • memories in these pathways can trigger relapse, hence why its so difficult to remain abstinent
18
Q

In cocaine addiction are there more D1 or D2 dopaminergic receptors?

A
  • D1 receptors
  • cocaine activates the reward pathway of mesolimbic system
19
Q

In cocaine addiction there are less D2 dopaminergic receptors. What can this then cause in patients for natural rewards?

1 - previous non-psychoaddcitve rewards no longer provide same reward stimulus
2 - patient more likley to seek cocaine to enhance reward pathways
3 - impact adversely on classic conditioning (memory/learning) and motivational states
4 - all of the above

A

4 - all of the above

20
Q

Opioid receptors are present throughout the mesocorticolimbic pathway, of which the locus coeruleus (LC), which in Latin means “blue spot” is part of. The LC is the principal site for brain synthesis of norepinephrine, a nucleus in the pons of the brainstem that is involved in stress and panic (fight or flight response). Opioids are able to reduce intracellular Ca2+ in the pre-synapse and increase K+ leaving the post-synapse, both of which cause hyperpolarisation. What do opioids generally do to the LC?

A
  • inhibit their firing
  • acute opioids = acute inhibition of LC
  • chronic opioids = LC neurons return to normal, linked with withdrawal from opioids
21
Q

What is the locus coeruleus, which in Latin means “blue spot”?

1 - nucleus in the pons of the brainstem responsible for dopamine synthesis
2 - nucleus in the pons of the brainstem responsible for the synthesis of norepinephrine
3 - nucleus in the pons of the brainstem responsible for the synthesis of corticol
4 - nucleus in the pons of the brainstem responsible for the synthesis of serotonin

A

2 - nucleus in the pons of the brainstem responsible for the synthesis of norepinephrine

  • principal site for brain synthesis of norepinephrine
  • involved in stress and panic (fight or flight response)
22
Q

Opioid receptors are present throughout the mesocorticolimbic pathway, of which the locus coeruleus (LC), which in Latin means “blue spot” is part of. The LC is the principal site for brain synthesis of norepinephrine, a nucleus in the pons of the brainstem that is involved in stress and panic (fight or flight response) and pain. Acute opioid use causes acute inhibition of the LC, but chronic activation of the opioid receptors leads to compensatory functional changes, this can lead to tolerance, why?

  • tolerance = desensitisation to a drug, meaning we need more of the drug for the same effects
A
  • LC develops tolerance to the inhibitory effect of opioids
  • LC begins firing and up-regulates in an attempt to return to normal
  • larger doses of opioids are required to inhibit this additional firing from the LC causing tolerance
23
Q

Opioid receptors are present throughout the mesocorticolimbic pathway, of which the locus coeruleus (LC), which in Latin means “blue spot” is part of. The LC is the principal site for brain synthesis of norepinephrine, a nucleus in the pons of the brainstem that is involved in stress and panic (fight or flight response) and pain. Acutely opioids inhibit the LC, but during chronic activation of the opioid receptors on the LC mean the LC goes into overdrive just to get back to normal levels. This can leads to compensatory functional changes and then dependance, why?

1 - cessation of opioids does not stop over activation of locus coeruleus (LC)
2 - no inhibition of LC by opiods leads to increased firing of LC and release of norepinephrine
3 - patients who stop taking opiods after becoming dependent will experience excessive fight or flight response, which is what withdrawal symptomns are.
4 - this can lead to a disturbance in physical homeostatic when the drug is removed
5 - all of the above

A

5 - all of the above

24
Q

If a patient is addicted to opioids, the aim is for complete absence. However, this is generally not possible and a treatment pathway should be used. What should be the first aim of a treatment plan?

1 - stop the drug and monitor the patient
2 - motivate the patient towards change and involve them in treatment plan
3 - start on a lower dose of opioids and slowly withdraw the drug

A

2 - motivate the patient towards change and involve them in treatment plan
- important to consider the stages of change model

25
Q

If a patient is addicted to opioids, the aim is for complete absence. However, this is generally not possible and a treatment pathway should be used. The first step is to try and motivate the patient towards change and involve them in treatment plan. What should be the next phase?

1 - stop the drug and monitor the patient
2 - motivate the patient towards change and involve them in treatment plan
3 - start on a lower dose of opioids and slowly withdraw the drug
4 - minimise harm related to taking substances, improve mental and physical health, reduce criminal activity and blood born infections

A

4 - minimise harm related to taking substances, improve mental and physical health, reduce criminal activity and blood born infections

26
Q

If a patient is addicted to opioids, the aim is for complete absence. However, this is generally not possible and a treatment pathway should be used. What should be the final phase of any treatment plan?

1 - stop the drug and use naloxone (opiod antagonist) and monitor the patient
2 - motivate the patient towards change and involve them in treatment plan
3 - start on a lower dose of opioids and slowly withdraw the drug
4 - minimise harm related to taking substances, improve mental and physical health, reduce criminal activity and blood born infections

A

1 - stop the drug and use naloxone (opiod antagonist) and monitor the patient

  • if the opiod cannot be stopped then it should be substited to a safer drug
27
Q

Alcohol is a suppressant, meaning it is able to reduce neuronal activity. What affected does alcohol have on GABA and glutamate receptors?

1 - GABA and glutaminergic = antagonist
2 - GABA = antagonist and Glutamine = agonist
3 - GABA = agonist and Glutamine = agonist
4 - GABA = agonist and Glutamine = antagonist

A

4 - GABA = agonist and Glutamine = antagonist

- generally large alcohol can inhibit most voltage gated channels

28
Q

Patients who associate alcohol with a positive valence (which increases dopamine release) and associate with a feeling of reward when consumed will have increased dopamine release from where?

1 - ventral tegmental area
2 - hypothalamuas
3 - locus coeruleus
4 - all of the above

A

1 - ventral tegmental area
- ventral tegmental area signals to the nucleus accumbens to release dopamine

29
Q

Patients who associate alcohol with a positive valence (which increases dopamine release) and associate with a feeling of reward when consumed will have increased dopamine release from the ventral tegmental area (VTA). What effect does alcohol then have on the VTA?

1 - NMDA (glutamate) antagonist of cortical input disinhibits VTA and increases dopamine
2 - GABA receptor antagonist of cortical input disinhibits VTA and decreases dopamine
3 - NMDA (glutamate) agonist of cortical input disinhibits VTA and decreases dopamine

A

1 - NMDA (glutamate) antagonist of cortical input disinhibits VTA and increases dopamine

  • causes an increase in dopamine release to the nucleus accumbens
  • means we continue to want alcohol to get the same effects
30
Q

In acute alcohol use what would we expect to see in GABA-A and NMDA receptors?

1 - GABA and NMDA agonist
2 - GABA and NMDA antagonist
3 - GABA agonist and NMDA antagonist
4 - GABA antagonist and NMDA agonist

A

3 - GABA agonist and NMDA antagonist
- agonist at GABA-A receptors
- antagonist at NMDA receptors
- influx of chloride and lack of Na+ entering cells means that the cell does not depolarise

31
Q

In chronic alcohol use what would we expect to see in GABA and NMDA receptors?

1 - GABA and NMDA receptors upregulated
2 - GABA and NMDA receptors downregulated
3 - GABA receptors downregulated and NMDA receptors upregulated
4 - GABA receptors upregulated and NMDA receptors downregulated

A

3 - GABA receptors downregulated and NMDA receptors upregulated
- down regulation of GABA-A receptors as alcohol is acting as an agonist so we dont need as many
- up-regulation of NMDA receptors as alcohol is an antagonist so we need more to increase sensitivity
- the increased NMDA receptors means the firing of NMDA receptors returns to a normal level as a compensatory mechanism

32
Q

In a patient who has alcohol withdrawal what could we see and why?

1 - upregulation of NMDA receptors causes an over excitation due to increases NMDA receptors
2 - alcohol acta as an antagonist to NMDA receptors, so if this inhibition is removed they will over shoot and continue to fire
3 - increase NMDA receptors and sensitivity results in physical symptoms (agitation, tremors, confusion, seizures)
4 - all of the above

A

4 - all of the above

33
Q

Which of the following is NOT a step in alcohol dependance?

1 - assessment (history)
2 - pyschoeducation (education, SMART goals)
3 - motivation for change (brief interventions, motiavtional interviewing)
4 - physcial examination

A

4 - physcial examination

34
Q

Which 2 of the following are the initial drugs that can be administered in a patient with alcohol withdrawal?

1 - benzodiazepines (GABA agonist)
2 - oral thiamine
3 - aytipcal antipsychotics
4 - codeine

A

1 - benzodiazepines (GABA agonist)
2 - oral thiamine

35
Q

Alcohol is a suppressant and In chronic alcohol ingestion the following occurs:

down-regulates the number GABA-A receptors
- down regulation of GABA-A is to increase neuronal firing

  • up-regulation of glutamate NMDA receptors
  • up-regulation of glutamate NMDA receptors is to increase neuronal firing above the suppression by GABA

In chronic alcohol ingestion what happens when the suppressor (alcohol) is removed?

1 - patient returns to normal function
2 - patient has lowered brain activity due to agonist affect of GABA
3 - increased fight or flight response causes physical symptoms
4 - all of the above

A

3 - increased fight or flight response causes physical symptoms
- bodies is primed for hypersensitivity to excitation above normal levels
- physical signs of hypersensitivity can be seen in a patients withdrawal symptoms (agitation, tremors, confusion, seizures)