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Pharmaceutical Care of Drugs (Mis)users > Chris Bailey Lectures > Flashcards

Chris Bailey Lectures Flashcards

1
Q

What does it mean to say a stimulus is reinforcing?

A

Something is reinforcing when an animal will perform a behaviour in order to obtain that stimulus. i.e. it is rewarding.

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2
Q

What is physiological dependence?

A

Cravings, compulsive drug use, loss of control, addiction.

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3
Q

What is physical dependence?

A

This is when stopping a drug causes a withdrawal syndrome. For example, the SSRI fluoxetine causes physical withdrawal symptoms if stopped abruptly but it is not addictive.

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4
Q

What are the two concentrations of dopaminergic neurons in the brain?

A

Ventral tegmental area -> frontal cortex + nuclues accumbens.

Substantia nigra –> Caudate (parkinsons)

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5
Q

What is the mesolimbic pathway?

A

This is the reward pathway, VTA –> nucleus accumbens.

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6
Q

What impact does ethanol have on dopamine release?

A

Increases it.

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7
Q

What impact does u-50 have on dopamine relase?

A

Decreases it. Disphoria.

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8
Q

What impact do imipramine and haloperidol have on dopamine release?

A

no impact.

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9
Q

How does cocaine increase dopamine levels?

A

Cocaine acts at the nerve terminal to inhibit the reuptake of dopamine from the synaptic cleft.

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10
Q

How does amphetamine increase dopamine levels?

A

Amphetamine acts at the nerve terminal to inhibit reuptake of dopamine and also to cause dopamine release.

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11
Q

How do opiates increase dopamine levels?

A

Opiates act on the mu-opioid receptors on GABAergic neurones.

This causes a disinhibition of DA neurones in VTA = more likely they will carry action potetial and release dopamine.

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12
Q

How does activation of the mu-opioid receptor lead to disinhibition of DA neurones?

A

Mu-opioid receptor = Gi/o coupled.

Gi/o = inhibits AMP –> cAMP.

Gi/o = inhibits Ca2+ channels, preventing Ca2+ into cell.

Gi/o = activates K+ channels, increasing K+ efflux.

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13
Q

How does ethanol increase dopamine levels?

A

Acts directly on DA neurones in VTA.

Decreases the AHP, increasing the firing rate = more dopamine relase.

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14
Q

Mu-opioid Gi/o activation results in ______ of Ca2+ transport _____ DA neurones.

A

Mu-opioid Gi/o activation results in inhibition of Ca2+ transport into DA neurones.

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15
Q

Mu-opioid Gi/o activation results in _________ K+ efflux from the DA neurone.

A

Increased, prevents hyperpolarisation?

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16
Q

Opiates act on ______ receptors on ______ neurones to cause a disinhibition.

A

Opiates act on mu-opioid receptors on GABAergic neurones.

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17
Q

Why does ethanol increase dopamine release?

A

It inhibits the potassium channels that are responsible for the after-hyperpolarisation, so the DA neurones are able to fire action potentials at a more rapid pace.

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18
Q

Why does alcohol use inhibit memory formation?

A

NMDA receptor antagonist

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19
Q

Why does alcohol impact balance?

A

Calcium channel antagonist.

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20
Q

Ethanol has what effect on GABAa?

A

Allosteric modulator of GABAa.

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21
Q

Why do people enjoy smoking? (pharmacologically)

A

Nicotine acts on nicotinic acetylcholine receptors on DA neurones in the VTA. This increases the firing rate and hence dopamine release and levels.

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22
Q

How does THC cause stimulation of the reward pathway?

A

THC acts on cannabinoid receptors on GABAergic neurones. CB1.

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23
Q

Why do sex and food stimulate the reward pathway?

A

Evolutionary approach to encourage behaviours which lead to propagation of genes.

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24
Q

Which route of administration causes the fastest peak of drug concentration in the brain?

A

Inhalation, not injection.

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25
Q

Which route of administration causes the slowest peak of drug concentration in the brain?

A

Ingestion.

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26
Q

Which is the better (in terms of time to peak conc) route of administration of a drug, snorting or injection?

A

Injection.
Order is:
Inhalation > Injection > snorting/stuffing > ingestion.

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27
Q

In terms of addiction, what is more important, the rate of dopamine release in the nucleus accumbens or the peak (total conc) attained from drug use?

A

The rate of dopamine release is more important, hence why injection and inhalation are associated with addiction.

28
Q

What is tolerance?

A

When continued use of a drug results in the need for increasing doses for equivalent effect.

29
Q

Which drugs of misuse does tolerance apply to most?

A

Opioids
Ethanol
Cannabinoids

30
Q

Why do people recently released from prison often die of overdose?

A

They have lost their tolerance during the time off drugs in prison. When they are released they attempt to take the same dose/amount and it is too much.

31
Q

What is the correlation between alcohol use and heroin overdose?

A

Heroin users often overdose with alcohol in their systems.

32
Q

Why do heroin users often overdose with alcohol in their systems?

A

Ethanol causes potential reversal of opioid tolerance and reversal of mu-opioid receptor desensitisation.

33
Q

Cardiac arrhythmias and psychosis are harms caused mostly by which drugs of abuse?

A

Psycho-stimulants.

34
Q

Infectious diseases result mostly from the use of what drugs and why?

A

Opiates - needles - blood sharing.

35
Q

How can alcohol withdrawal be treated pharmacologically? (3)

A
  1. Benzodiazepines
  2. Anti-epileptics
  3. Antipsychotics
36
Q

How can opitate withdrawal be treated pharmacogically?

A
  1. Clonidine - alpha agonist.
  2. Benzodiazepeines
  3. Sedation
  4. Replacement therapy e.g. methadone, buprenorphine.
37
Q

How can nicotine withdrawal be treated?

A

Replacement therapy.

38
Q

Why is the relapse rate for drug addicts so high?

A

Replacement therapies do not solve the addication/psychological dependence issues. 80% relapse.

39
Q

What is varenicline?

A

Partial agonist of the nicotine receptors - provides partial relief.

40
Q

Why is it harder to overdose via buprenorphine than methadone?

A

Buprenorphine is only a partial agonist plus it is only administered via a patch or buccaly.

41
Q

What is aversion therapy for alcohol abuse based around?

A

The use of disulfiram.

42
Q

How does disulfiram work?

A

Disulfiram works by inhibiting the enzyme acetaldehyde dehydrogenase, which means many of the effects of a “hangover” are felt immediately after alcohol is consumed.

43
Q

What is a major problem relating to the use of naloxone/buprenorphine/naltrexone etc?

A

They prevent pain relief in event of injury.

44
Q

How is the issue of compliance regarding opioid antagonists being addressed?

A

Drug Depots in the skin - some drug users will dig these out however.

45
Q

What are the 3 major stimuli for relapse in humans?

A
  1. Taking a small dose of the drug.
  2. Stress
  3. Being presented with a cue that reminds the person of drug taking - music, BBQ smell etc.
46
Q

In a drug user, how is the euphoric effect associated with a drug and the dysphoric effect of a comedown different to a drug niave person?

A

The euphoric effect becomes blunted - more drug for same effect.
The dysphoric effect becomes exaggerated when not on drug/on comedown.

47
Q

What enzyme does disulfiram inhibit, what does this cause?

A

It inhibits acetaldehyde dehydrogenase = meaning effects of hangover are felt straight away.

48
Q

When a person is dependent on a drug, what can be said about the effect the drug has on their baseline level of happiness?

A

It simply returns it to a normal level - experienced by everyone else.

49
Q

How is it thought that repeated withdrawal affects baseline mood?

A
  1. Dysregulation of stress hormones

2. Increased production of dynorphin

50
Q

What is antalarmin?

A

Antalarmin is a non-peptide drug that blocks the CRF-1 receptor, and, as a consequence, reduces the release of ACTH in response to chronic stress.

51
Q

How does dynorphin result in reduced baseline happiness levels?

A

Dynorphins exert their effects primarily through the κ-opioid receptor (KOR), a G-protein-coupled receptor.

Dynorphin decreases dopamine release by binding to KORs on dopamine nerve terminals.

52
Q

Why might kappa opioid receptor antagonists be a future drug treatment for addiction?

A

Dynorphin decreases dopamine release by binding to KORs on dopamine nerve terminals.

53
Q

What is the relationship between levels of D2 receptors and drug abuse?

A

Those with fewer receptors appear to use drugs more - rat studies.

54
Q

Recovered addicts have less of what type of receptor in the NAcc?

A

D2.

55
Q

Long term cocaine use in monkeys reduces the levels of what receptor in the accumbens?

A

D2.

56
Q

How does Buprion work?

A

Dopamine/noradrenaline reuptake inhibitor - may just work in addiction because it is an antidepressant.

57
Q

What is bromocriptine?

A

Partial D2 agonist.

58
Q

Addiction is what type of behaviour?

A

Learned.

59
Q

Why could inhibiting synaptic plasticity (and therefore memory formation) be useful in addiction treatment?

A

Memory formation is thought to occur because of synaptic plasticity, particularly at glutamatergic synapses. Inhibiting this = inhibits conditioned learning.

60
Q

How can interfering with memory formation be used to treat people who are already addicts?

A

By interfering with the process of reconsolidation.

61
Q

What is reconsolidation?

A

Reconsolidation is the process of strengthening memory.

62
Q

Why does disrupting reconsolidation extinguish memory?

A

Without the reconsolidation and synaptic plasticity memories are not reactivated and retained.

63
Q

Therapy that seeks to make addicts forget they are addicted would involve:

A

Re-exposure of addicts to cues related to their addiction.

Use of agents that interfere with memory formation: propranolol.

64
Q

Current drug treatments are based around what? [4]

A
  1. Replacement therapy.
  2. Aversion therapy
  3. Antagonists
  4. Bupropion/Bromocriptine
65
Q

Future drug treatments for abuse are based around what? [4]

A
  1. Antibodies
  2. Stress hormone antagonists
  3. Kappa opioid receptor antagonists
  4. Agents that affect memory

Pharmaceutical Care of Drugs (Mis)users (12 decks)

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