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(UNI) Neuropharmacology (3rd Year) > Drugs of Abuse > Flashcards

Drugs of Abuse Flashcards

1
Q

Define drug abuse.

A

Drug abuse is repeated non-medicinal use of bit prescription or non-prescription drugs for pleasure or sporting gain.

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2
Q

List the categories of drugs which are frequently abused, with examples.

A

Psychostimulants (cocaine/amphetamines), depressants (barbiturates/alcohol), psychotomimetics (LSD/cannabis), opiates (heroin/dihydrocodeine), volatile intoxicants (glue), Legal highs (spice).

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3
Q

Give examples of psychostimulants.

A

Cocaine, amphetamines, nicotine.

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4
Q

Give examples of depressants.

A

Barbiturates, alcohol.

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5
Q

Give examples of psychotomimetics.

A

LSD, PCP, cannabis.

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6
Q

Give examples of opiates.

A

Heroin, dihydrocodeine.

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7
Q

Give examples of volatile intoxicants.

A

Glue, amyl nitrate.

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8
Q

Give examples of legal highs.

A

Spice.

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9
Q

Describe the characteristics of psychological dependence.

A

Drug seeking behaviour, pleasure (positive reinforcement), not related to the development of tolerance, drug habit (environment and old habits reengage drug seeking behaviour).

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10
Q

Describe the characteristics of physiological dependence.

A

The body needs the drug for normal function, tolerance and sensitisation, physical withdrawal symptoms (negative reinforcement).

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11
Q

Define tolerance.

A

Physiological chamges that allow one to take more of the drug; a compensatory response.

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12
Q

Define sensitisation.

A

An increase in the amount of drug needed to feel high.

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13
Q

Define cross tolerance.

A

Cross Tolerance is where tolerance to one drug causes tolerance to another within the same class.

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14
Q

Define drug withdrawal.

A

This is a drug-specific syndrome that occurs when drug supply is abruptly terminated. Symptoms of withdrawal are usually the opposite of the effects of the drug before the user became tolerant. Examples of this are the heroin ‘cold turkey’ and the cocaine ‘crash’.

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15
Q

Where do drugs of abuse act? Why is this area good for these drugs to work?

A

Drugs of abuse act in the brain. The mesolimbic dopamine pathway is directly involved (this includes the nucleus accumbens, ventral tegmental area, and the prefrontal cortex). This is the perfect place as the brain already has pre-existing reward systems such as those for food, water, sex, and social interaction. These reward systems have evolved to encourage behaviour with a positive effect on Darwinian Fitness.

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16
Q

What neurotransmitters are involved in addictive drugs of abuse?

A

All addictive drugs of abuse activate dopamine release in the shell of the NAc. Some directly through release of DA and some indirectly through suppression of GABA inhibition of DA cells.

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17
Q

What compound is cocaine structurally related to? How do they have similar actions in nature?

A

Cocaine is structurally related to atropine as they are both plant-based alkaloids evolved by the plant as a form of protection.

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18
Q

What is crack?

A

Crack is water-insoluble cocaine without HCl, which is removed using bicarbonate and water so that it is smokable. Crack is very potent as it is very fat soluble.

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19
Q

Describe the action cocaine has on the CNS.

A

Cocaine blocks the CNS dopamine transporter (DAT), this increases ambient dopamine in the nucleus accumbens by preventing its reuptake. This allows there to be more dopamine to act in the cleft.
Cocaine also blocks serotonin and noradrenaline reuptake, but with lower affinity.

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20
Q

Does cocaine produce tolerance and/or sensitisation?

A

Cocaine produces rapid tolerance with long term sensitisation.

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21
Q

What are the withdrawal symptoms of cocaine?

A

The withdrawal symptoms include dysphoria (‘crash’), depression, intense anxiety, and psychological craving.

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22
Q

What are amphetamines structurally similar to?

A

Noradrenaline.

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23
Q

How do amphetamines differ from catecholamines?

A

They are more lipid soluble than catecholamines so are penetrate the brain to a greater degree and stay in place for longer.

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24
Q

List three different forms of amphetamines.

A

MDMA, methamphetamine, amphetamine.

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25
Q

List some of the uses that amphetamines were once used for.

A

Decongestant, anorectic, pro-vigilant.

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26
Q

What are the effects of amphetamine toxicity?

A

Chronic use causes paranoid psychosis and amphetamine-specific necrotizing arthritis (brain haemorrhage, kidney failure). The chemicals used for the production of amphetamines can also lead to lead poisoning.

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27
Q

What effect can amphetamine have on the brain?

A

Amphetamine use makes the brain more intensely wired.

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28
Q

How long does the high from meth last? What effect does it have?

A

The high lasts for 8-24 hours. It prevents behavioural inhibition, leading to outrageous and odd behaviour.

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29
Q

What is formication?

A

Formication comes from the French word for ants (formi) as it is the sensation of insects crawling under the skin. This is caused by increased core temperature, sweating, and dehydration, as well as loss of skin oils. This combined with powerful tactile delusions lead to these delusions.
These delusions lead to the user trying to get rid of the ‘insects’ by cutting them out.

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30
Q

How does MDMA work?

A

MDMA blocks the 5-HT transporter, causing an increase in ambient 5-HT, as well as causing the transporter to work in reverse, pumping 5-HT into
the synaptic cleft. Both of these effects lead to a large increase in ambient serotonin.

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31
Q

What are the long term toxic effects of MDMA?

A

In the long term, users suffer from presynaptic degeneration, chronic depression, and memory & cognitive impairment.

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32
Q

What are the short term toxic effects of MDMA?

A

In the short term, users suffer from serotonin depletion causing dysphoria, depression, and severe acute hyperthermia (overheating).

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33
Q

What is methylphenidate used for?

A

This is a drug that is given to children with ADHD, it is often known by the brand name Ritalin.

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34
Q

How does methylphenidate work?

A

This is a weak DA, NA uptake inhibitor with no effect on 5-HT. It is much more effective on mental activity compared to motor activity.

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35
Q

List the effects of nicotine.

A

Increased alertness. Facilitation of memory and attention. Reduced appetite. Tremor, muscle relaxation. Nausea. Increased respiration. Tachycardia. Hypertension. Increased GI motility.

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36
Q

At high doses, such as those associated with toxicity, what are the effects of nicotine?

A

Depolarising blockade of the neuromuscular junction and autonomic ganglia. Possible death by cardiac collapse and respiratory failure.

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37
Q

How is nicotine overdose/toxicity treated?

A

Treatment for this is gastric lavage (stomach pumping) and general support measures.

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38
Q

How does nicotine work?

A

Nicotine causes increased dopamine release in the NAc, increasing NAc GABA output to the VTA. It acts pre-synaptically to increase dopamine release and post synaptically to increase dopamine neurone firing, triggering burst firing. Nicotine acts only at nAChR containing β2 subunit. Nicotine also excites cholinergic interneurons in the NAc into burst firing mode, an important component of addiction.

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39
Q

How are Chinese smokers different from other ethnicities?

A

Chinese smokers metabolise nicotine slower, therefor smokes less, therefor are less likely to die.

40
Q

List the effects of alcohol abuse.

A

Hepatic cirrhosis. Alcoholic hepatitis. Renal damage. Oral and throat cancer. Korsakoff’s syndrome – caused by a lack of thiamine (B1) (Anterograde amnesia, Dementia).

41
Q

How does alcohol act on NMDA receptors?

A

Allosteric inhibitor, increased NMDAR over time leading to physical dependence and withdrawal.

42
Q

How does alcohol act on GABA-A receptors?

A

Allosteric factor, causes tolerance.

43
Q

How does alcohol act on 5-HT-2/3 receptors?

A

Positive modulator – sedative, antianxiety, euphoric effects.

44
Q

How does alcohol act on L-type calcium channels?

A

Allosteric inhibitor.

45
Q

How does alcohol act on nACh receptors?

A

Positive modulator.

46
Q

How does alcohol act when consumed with cannabis?

A

Alcohol shows cross tolerance with cannabis; it increases the effects of n-arachidonyl ethanolamide, an agonist at CB1R, increasing its synthesis.

47
Q

What are barbiturates used as?

A

They are used as hypnotics and sedatives (e.g. in surgery).

48
Q

Why have barbiturates been replaced in main line use?

A

They have a narrow therapeutic window, they are toxic at only 10x the hypnotic dose hence they have been replaced by benzodiazepines.

49
Q

What are the withdrawal symptoms associated with barbiturates?

A

Withdrawal symptoms include anxiety, vomiting, hyperthermia, and seizures.

50
Q

How do barbiturates work?

A

Barbiturates act at GABAA receptor channels, on the β1 subunit. This prolongs the GABA opening of Cl- channels, leading to more Cl- passing through the channel.

51
Q

In the 1950s/60s, what were benzodiazepines used for?

A

Anxiolytics (stress and situational depression) and sedatives.

52
Q

What are the withdrawal effects of benzodiazepines?

A

Withdrawal after prolonged abuse induces anxiety, nausea, and insomnia.

53
Q

What novel and dangerous way did Scottish benzodiazepine addicts use to get their fix in the 1990s?

A

Users would inject melted temazepam caplets (jellies) which was the cause of significant limb amputations.

54
Q

List commonly used benzodiazepines.

A

Midazolam, triazolam, temazepam, lorazepam, diazepam.

55
Q

How do benzodiazepines work?

A

Benzos bind to the α-subunit of the GABAA receptor, increasing the frequency of opening of the channel, not duration, hence more GABA activity leading to CNS depression. They may release dopamine through disinhibition.

56
Q

What is the chemical name of rohypnol, its physical properties, and its use.

A

Flunitrazepam. Odourless and colourless. Used as a date rape drug.

57
Q

What drug has overtaken rohypnol in use as a date rape drug?

A

GHB.

58
Q

What endogenous compound is GHB a derivative of?

A

GABA.

59
Q

How does GHB work?

A

It activates GABAA receptors on presynaptic terminals to reduce GABA and glutamate release.

60
Q

What is GHB used to treat?

A

Alcohol withdrawal.

61
Q

What does opium resin contain?

A

Morphine, codeine, noscapine, papaverine, thebaine.

62
Q

Who first synthesised heroin? What did he test it on?

A

Heroin was first synthesised by Hoffman in 1898 and he tested it on sticklebacks.

63
Q

List the desirable effects of opioid use.

A

The desirable effects of opioid use include euphoria, sedation, relief of anxiety and analgesia. Subjective effects include limb heaviness, lethargy, and warmth.

64
Q

List the undesirable effects of opioid use.

A

Undesirable effects include constipation and nausea.

65
Q

List the withdrawal symptoms of opioids?

A

Sweating, aching, nausea, and vomiting.

66
Q

List the effect of long term opioid use.

A

Respiratory depression (leading to OD). Heroin lung (oedema). Venous collapse.

67
Q

How do opioids work?

A

The brain produces endorphins and enkephalins which are endogenous opioids. Opiates act at the receptors for these compounds, opioid receptors. Opiates produce a massive dopamine release in the NAc through inhibition of GABA release onto cells in the VTA (disinhibition).

68
Q

How do opioids effect neurones?

A

Opioids reduce the connections between neurones.

69
Q

How more potent than morphine is fentanyl?

A

1,000x.

70
Q

How more potent than morphine is carfentanyl?

A

10,000x.

71
Q

How more potent than morphine is krokodil?

A

10x.

72
Q

How long is the half life of krokodil?

A

1.5hr.

73
Q

How long is the half life of morphine?

A

4-6hr.

74
Q

Define psychotomimetics.

A

These are mind altering drugs such as LSD, cannabis, PCP, and mushrooms; they cause hallucinations. These substances have been known since antiquity, where they were often used for shamanic rituals.

75
Q

What are the active compounds in cannabis?

A

THC (tetrahydrocannabinol), CBD (cannabidiol).

76
Q

What purpose did THC evolve for?

A

THC was evolved as a plant defensive mechanism; it is a glue-like substance which ‘glues’ the mouths of attacking insects shut and ‘glues’ them to the plant so birds and other predators can eat them.

77
Q

How can cannabis be potentially used to help cancer patients?

A

It has also been shown to have anti emetic properties which are useful in the treatment of nausea and vomiting associated with cancer chemotherapy.

78
Q

What are the effects of heavy cannabis use?

A

Heavy cannabis use can lead to cannabinoid psychosis, delusions, and paranoia.

79
Q

How does THC work?

A

THC binds to CB1R receptors in the brain and CB2R receptors in the periphery. There are lots of CB1R receptors in the limbic system and the mesolimbic nuclei. G-coupled CB1 receptors are found on inhibitory (GAB) presynaptic terminals and their activation leads to a profound depression of GABA release. In the VTA this leads to dopamine release in the NAc.

80
Q

How does LSD work?

A

LSD acts as a partial agonist at the 5-HT2 receptors, but also at NA and dopamine receptors to some extent, whilst inhibiting 5-HT release. The Raphe activating system is critical for its action, as is the NAc for its dopamine action.

81
Q

How does LSD affect the user?

A

Taking LSD mimics dream-state biochemistry (low 5-HT drive and higher cholinergic activity) in a hyper aroused individual. This causes auditory and visual illusions known as synaesthesia.

82
Q

What are the short term bad effects of LSD?

A

Heavy anxiety, horrific illusions.

83
Q

What are the long term bad effects of LSD?

A

Psychosis.

84
Q

How do PCP and ketamine work?

A

They are dissociative anaesthetics which inhibit the 5-HT and NA reuptake mechanisms as well as inhibiting NMDA glutamate receptors.

85
Q

What is the toxicology of PCP and ketamine?

A

Brain damage. PCP vacuolates neurones. Induced apoptosis (neuronal suicide). Severe, possibly irreversible, psychosis.

86
Q

How do volatile substances work?

A

These substances act similarly to anaesthetics, altering neuronal membrane stability.

87
Q

What is the toxicology of volatile substances?

A

Significant risk of sudden death due to cardiac arrest or blood oxygen depletion (amyl nitrate, butane).
Peripheral and central neuropathy (hexane). Hearing and sight loss (toluene). Bone marrow damage (benzene).

88
Q

List commonly abused anticonvulsants.

A

Gabapentin, pregabalin.

89
Q

What are the street names of synthetic cannabinoids?

A

Black mamba, exodus damnation, K2, and spice.

90
Q

How do synthetic cannabinoids make users feel?

A

These substances produce hypothermia and bradycardia as well as a feeling of oblivion; deleting life for a bit.

91
Q

How do synthetic cannabinoids work?

A

These compounds bind at type 1 cannabinoid receptor CB1R. They are highly lipophilic so are long acting as they hang around for so long. Their EC50 is often low nM, driving massive CB1R activity. This has effects on GABA inhibition.

92
Q

List the side effects of synthetic cannabinoids.

A

Abulia. Psychosis. Hypothermia. Catatonic state (stupor, mutism, unresponsiveness). Catalepsy (maintenance of an uncomfortable, ridged posture (a feature of catatonia)).

93
Q

What are the street names of mephedrone?

A

MCAT, meow meow.

94
Q

How does mephedrone work?

A

There mechanism causes a 500% increase in dopamine release in the NAc and a 950% increase in 5-HT release.

95
Q

What is bruxism?

A

Grinding of the teeth.

(UNI) Neuropharmacology (3rd Year) (20 decks)

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