Lecture 15- Inhalants and GHB Flashcards

1
Q

What are inhalants?

A

Volatile liquid/gases that readily vaporize.

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2
Q

What are the 3 types of inhalant compounds?

A

Volatile Solvents: liquid at room temperature, give off fumes
Aerosols: Contain solvents/propellants Gases: Can be sniffed/inhaled/sprayed into the mouth

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3
Q

What are the acute effects of inhalants?

A

euphoria, disinhibition, simulation then light-headedness

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4
Q

What are the effects of heavy exposure to inhalants?

A

Slurred speech, hallucinations, delusions.

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5
Q

What are the effects of high doses of inhalants?

A

Anaesthesia, coma

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6
Q

What are the origins of inhalants?

A

-Ancient use linked to mystical practices and spiritual leaders inhaled fumes from incense and oils to alter consciousness. - Nitrous oxide was regarded as a cheap substitute for alcohol and was popularized by the British scientist Sir Humphry Davy

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7
Q

Why is little known about the neural mechanisms of inhalants?

A

Less is known about neurochemical activation as only recently used for recreational purposes.

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8
Q

How are the effects of inhalant mediated in the brain?

A

-Rapidly absorbed, fat soluble -Distributed widely around brain esp. striatum, thalamus

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9
Q

How addictive are inhalants?

A

-Dopamine is common across addictive drugs and is the substrate of normal reward systems -Mesolimbic pathway is implicated in natural reward and drug abuse.

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10
Q

How did the Funada et al (1992) study test addictiveness of inhalants?

A

-Study conducted on mice in two connected chambers, toluene is distributed in one of two chambers. - Mice show preference for toluene chambers than non-toluene chamber, where before administration of the substance they showed no preference of either chamber.

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11
Q

How do inhalants affect CNS excitability?

A

-Inhalants enhance function of GABA & glycine inhibitory receptors
-Inhalants inhibit excitatory NMDA glutamate receptors

Similar to alcohol as reduce CNS excitability

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12
Q

What are the 2 disorders caused by adverse effects of stimulants?

A

Sudden sniffing death syndrome (SSDS)
Deadly Blood disorder

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13
Q

What is Deadly Blood disorder/

A

Result from inhaling nitrates or poppers which is where the blood becomes physically changed so that it can’t deliver oxygen to the body.

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14
Q

What is Sudden sniffing death syndrome (SSDS)?

A

Caused from use of inhalants leading to sudden rapid heart rhythms or irregular heart rhythms.

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15
Q

What are the legal issues involved with inhalants?

A

Solvent misuse isn’t illegal - although it’s illegal in England and Wales for shopkeepers to sell intoxicating substances to those ‘likely’ to be inhaling them.

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16
Q

What is the background of GHB?

A

-One of the two most common date rate drugs along with Rohypnol.
-Closely related to GABA (inhibitory neurotransmitter)

17
Q

What can GHB be used to clinically treat?

A

Cataplexy
(sudden loss of muscle control experienced by narcoleptics)

18
Q

What is GHB?

A

It is a natural product of human metabolism. It is a carbohydrate found in abundance in our diet as animal meat contains GHB, as does wine and small citrus fruits. It is also biologically synthesized from GABA an amino acid that is structurally similar to GHB.

19
Q

What are the 3 forms of GHB?

A

-Colourless, tasteless liquid -Blue coloured liquid -Crystals/powder (less common)

20
Q

What are the behavioural effects of GHB?

A

-Effects are felt within 15mins and last 3 or 4 hours -Relaxation, drowsiness, sociability, euphoria, tunnel vision, hallucinations

21
Q

How is dopamine connected to GHB in the neural mechanisms?

A

Dopamine associated with most drugs and leads to reinforcement. Targets the mesolimbic pathway, induced a sense of reward through dopamine release, thus becomes reinforcing

22
Q

How is GABA connected to GHB in neural mechanisms?

A

GABA is an inhibitory neurotransmitter, which explains some of the behaviour effects of GHB, e.g. sense of relaxation.

23
Q

What are the 2 neural mechanisms of GHB?

A

1)GBH mediates pre and post synaptic GABA release

2)GHB effects are mediated by specific GHB receptors. These receptors would respond to both naturally produced GHB and chemically produced GHB, thus excess of this substance causes a ‘high’

24
Q

What are the effects of chronic GHB use?

A

There is little info regarding long term effects but some suggest it can lead to memory problems, heart disease, hallucinations.

25
Q

What do experiments from rats suggest about chronic GHB use?

A

Some evidence from rats that long term exposure can lead neurological damage, affecting the ‘grasping’ reflex, as well as alteration in spatial and working memories (Pedraza et al., 2009).

26
Q

What does Zeng et al (2002) say about adverse effects of GHB?

A

Participants were significantly slower on behavioural tasks that other addicted groups and healthy controls

-Particularly bad at visuospatial, executive function, and memory tasks.

27
Q

What are withdrawal symptoms of GHB?

A

Symptoms reported as insomnia, anxiety and tremors, and at high doses even hallucinations, delirium, extreme agitation and psychosis

28
Q

What are the legal issues of GHB?

A

Gained reputation as club/date rape drug

29
Q

What are the clinical applications of GHB?

A

In both Narcolepsy (sleep attacks) and Cataplexy (muscle weakness) a systematic review found GHB was effective in treating but the medication was not well tolerated.