Inhalants and GHB Flashcards
What is GHB?
The ‘date rape’ drug.
What are inhalants?
Abused volatile liquid or gases at room temperature that do not belong to any other defined class, often from everyday household items.
What are the different ways of using inhalants?
- Sniffing fumes
- Inhaling from a balloon
- Inhaling from a saturated rag
- Inhaling from a plastic or paper bag
- Aerosol cans
What are some common inhalants?
Acetone, aliphatic and aromatic hydrocarbons, BCF, n-Butane, butanone (adhesives).
The main three categories of inhalants are:
Volatile:
- solvents (liquid at rt, give off fumes)
- aerosols (sprays containing solvents and propellants)
- gases (domestic or anaesthetic)
All euphoriants.
What are the acute behavioural effects of inhalants?
Euphoria, disinhibition, stimulation.
Then light-headedness and drowsiness (like with alcohol).
What are the behavioural effects of heavy exposure to inhalants?
Slurred speech, ataxia, lethargy, hallucinations and sometimes delusions.
What are the behavioural effects of very high doses of inhalants?
Anaesthesia and coma.
Why do users tend to repeat doses of inhalants?
Because the hit is quite short.
What effects can inhalants leave afterwards?
A ‘hangover’ and sometimes a red rash around the mouth.
What are the risks of inhalants?
- Tolerance and withdrawal syndrome = dependence.
- Sudden sniffing death syndrome from cardiac arrhythmia
- Damage to lungs, kidneys and liver
- Subcortical brain anomalies
- Damage to myelin
- Vomiting and blackouts
What are the specific risks associated with taking inhalants in a certain way?
- Squirting down the throat - can cause throat to swell, restricting breathing and slowing the heart.
- Inhaling from a bag - suffocation risk
- Using in combination with alcohol leads to an increased risk of death.
What did Rosenberg et al (2002) find about drug-related subcortical anomalies?
Increased risk of anomalies with inhalants compared to other drugs in the basal ganglia, cerebellum, pons and thalamus. Up to about 40% of users had anomalies.
Is solvent misuse illegal?
No, but illegal for shopkeepers to sell to people they think will inhale them.
In the US, at what age does solvent abuse tend to start and peak?
Can start as early as in 7 year olds, peaks in 10-12 year olds.
What did Funada et al (1992) find about the rewarding effects of toluene in mice?
Two compartments, in training phase one filled with toluene the other air, then in test phase observed how long spent in each chamber. Mice showed significant preference for the toluene chamber and controls showed no preference.
Inhalants are rapidly absorbed and distributed widely around the brain. What areas of the brain are inhalants concentrated in?
The striatum, thalamus and deep cerebellar nuclei, as shown by Gerasimov et al (2002) with a baboon imaging study.
What are the neural effects of inhalants?
Depressant effects - enhance function of GABA and glycine inhibitory receptors and inhibit excitatory NDMA glutamate receptors. This is a similar effect to alcohol, as it reduces CNS excitability. Dopamine may also be released, leading to reinforcement.
What does GHB stand for?
Gamma hydroxybutyrate.
When is GHB often used?
It’s a ‘club drug’ like ecstasy and ketamine, and is notorious for its use as the ‘date rape’ drug.
What is the clinical use of GHB?
Used to treat cataplexy in narcoleptics.
What other drugs are used in date rape, in addition to GHB?
Ketamine (hallucinogen) and rohypnol (benzodiazepine).
What are the behavioural effects of low doses of GHB?
Mild euphoria, disinhibition and relaxation.
What are the behavioural effects of high doses of GHB?
Slurred speech, ataxia, lehargy, dizziness, nausea and vomiting.
What are the effects of overdosing on GHB?
Respiratory depression, loss of consciousness and seizures.
What is the evidence for GHB tolerance?
- Informal reports of increasing dose
- Withdrawal symptoms - insomnia, anxiety and tremors (or even hallucinations, delirium, extreme agitation and psychosis).
- Funada et al (2002) found tolerance to locomotor-suppressant effects in mice.
How was GHB first discovered and used?
- Discovered when looking for a GABA analogue to use as a CNS depressant for use as a sedative or anaesthetic.
- Initially sold in US health shops as a supplement for body builders to reduce fat and increase muscle, but adverse effects = ban.
What are the behavioural effects of GHB in lab animals?
- Lower doses - sedation, reduced locomotor activity, decreased anxiety.
- Higher doses - cataplexy and CNS excitation (like petit mal seizures in humans?)
Why do people take GHB?
Because of its reinforcing effect (although animal studies inconsistent): Funada et al (1992) place conditioning task in rats and mice showed reinforcing effect, but IV self-administration in monkeys didn’t. Some sedated themselves (either unpleasant or too drowsy to get more?).
What are the different (vague!) hypotheses as to the neural effects of GHB?
- Acts (weakly) on GABAB receptors/is metabolised into GABA.
- There’s a GHB receptor - selective binding sites, GHB analogue selective antagonist.
What is the evidence for and against GHB acting on GABAB receptors?
- Has little effect on GABAA receptors.
+ GHB effects counteracted by GABAB antagonists (Carter et al, 2003).
What is the evidence for and against GHB being a neurotransmitter with its own receptors?
+ GHB = nt synthesised from GABA
- Endogenous GHB levels not behaviourally effective = different mechanism
- Not all GHB effects blocked by antagonist.
+/-/? At high doses GHB receptor antagonist acts like an agonist.
