Opioids

Revision as of 02:48, 27 February 2018 by >Pjb (Grammatics)

Fatal overdose may occur when opiates are combined with other depressants such as benzodiazepines, barbiturates, gabapentinoids, thienodiazepines, alcohol or other GABAergic substances.[1]

It is strongly discouraged to combine these substances, particularly in common to heavy doses.

An opioid is any psychoactive chemical that resembles morphine or other opiates in its pharmacological effects. Opioids work by binding to opioid receptors, which are found principally in the central and peripheral nervous system and the gastrointestinal tract.[citation needed] The receptors in these organ systems mediate both the beneficial effects and the side effects of opioids.

Common substances that affect the u-opioid receptor: morphine, codeine, diacetylmorphine (Heroin), naloxone (Narcan), methadone, tramadol.
Poppy pod scored to release opium latex
Dried pods for preparation of tea or solvent extraction of alkaloids

Although the term opiate is often used as a synonym for opioid, the term opiate is limited to drugs derived from the natural alkaloids found in the resin of the opium poppy (Papaver somniferum)[2]. While opioid is a more general term for substances that act primarily on opioid receptors, including natural occurring alkaloids, synthetic substances and opioid peptides [3].

Opioid dependence can develop with ongoing administration, leading to a withdrawal syndrome with abrupt discontinuation.[4] Opioids are not only well known for their addictive properties, but also for their ability to produce a feeling of euphoria, motivating some to use opioids recreationally.

Chemistry

Opioids are based upon morphine and opium-like structures. They work via their similar chemical structures to the endogenous opioids in the body. Morphine derived opioids, known as morphinans, contain a benzene ring attached to two partially unsaturated cyclohexane rings (phenanthrene) and a 4th nitrogenous ring attached to the core at carbons 9 and 13. There are several classes of opioids which differ greatly in structure from each other. For example, fentanyl and its analogues are structurally unique from morphinans and tramadol derivaties.

Pharmacology

 
Metabolic pathway of codeine and morphine courtesy of Pharmgkb.org

Opioids are known to mimic endogenous endorphins. Endorphins are responsible for analgesia (reducing pain), causing sleepiness, and feelings of pleasure. They can be released in response to pain, strenuous exercise, orgasm, or excitement.[citation needed] This mimicking of natural endorphins results in the drug's euphoric, analgesic (pain relief) and anxiolytic (anti-anxiety) effects.

Receptor types

Opioids act on the three main classes of opioid receptor in the nervous system, μ, κ, δ (mu, kappa, and delta). Each opioid is measured by its agonistic or antagonistic effects towards the receptors, with the responses to the different receptor sub-types (e.g., μ1 and μ2) providing even more effects. Opioid receptors are found mainly within the brain, but also within the spinal cord and digestive tract. [citation needed]

Delta (δ)

The delta receptor is responsible for the analgesia, antidepressant and convulsant effects as well as physical dependence.[citation needed]

Kappa (κ)

The kappa receptor is responsible for the analgesia, anticonvulsant, dissociative and deliriant effects as well as dysphoria, neuroprotection and sedation.[citation needed]

Mu (μ)

The mu receptor is responsible for analgesia, physical dependence, respiratory depression, euphoria, and possible vasodilation.[citation needed]

Nociceptin

The nociceptin receptor is responsible for anxiety, depression, appetite and development of tolerance to μ agonists.[citation needed]

Zetta (ζ)

The zetta opioid receptor, also known as opioid growth factor receptor (OGFr) is responsible for tissue growth, neural development, and is further implicated in the development in some cancers. The endogenous ligand for OGFr is met-enkephalin, which is also a powerful endogenous delta opioid receptor agonist.[citation needed]

Subjective effects

Disclaimer: The effects listed below cite the Subjective Effect Index (SEI), an open research literature based on anecdotal user reports and the personal analyses of PsychonautWiki contributors. As a result, they should be viewed with a healthy degree of skepticism.

It is also worth noting that these effects will not necessarily occur in a predictable or reliable manner, although higher doses are more liable to induce the full spectrum of effects. Likewise, adverse effects become increasingly likely with higher doses and may include addiction, severe injury, or death ☠.

Physical effects
 

Cognitive effects
 

Visual effects
 

Pharmacological classes

Naturally occuring
 

Semi-synthetic
 

Toxicity and harm potential

In non-chronic use of safe dosages of opioids, physical and neurological toxicity are markedly safe.[citation needed]

Long term effects

Long term use of opioids causes hormonal imbalance in both men and women.[5]

In men, this opioid-induced androgen decificeny essentially means that a long-term male opioid user will produce less than normal amounts of sex hormones – especially testosterone.[6]

This negative change in endocrine function in males can lead to:

  • Reduced libido
  • Erectile dysfunction
  • Fatigue
  • Depression

A long term male user may also find more visual effects of their lowered testosterone such as:

  • Reduced facial and body hair
  • Decreased muscle mass
  • Weight gain

It is strongly recommended that one use harm reduction practices when using this class of substances.

Tolerance and addiction potential

Due to the highly euphoric nature of these substances, the recreational use and abuse of opioids has an extremely high rate of addiction and dependence. This is combined with a tolerance which builds up quickly, necessitates that the user take increasingly high dosages in order to get the same effects.

The risk of fatal opioid overdoses rise sharply after a period of cessation and relapse, largely because of reduced tolerance.[7] To account for this lack of tolerance, it is safer to only dose a fraction of one's usual dosage if relapsing. It has also been found that the environment one is in can play a role in opioid tolerance. In one scientific study, rats with the same history of heroin administration were significantly more likely to die after receiving their dose in an environment not associated with the drug in contrast to a familiar environment.[8]

See also

References

 

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  1. Risks of Combining Depressants - TripSit 
  2. Hemmings, Hugh C.; Egan, Talmage D. (2013). Pharmacology and Physiology for Anesthesia: Foundations and Clinical Application: Expert Consult - Online and Print. Elsevier Health Scienc,es. p. 253. ISBN 1437716792. Opiate is the older term classically used in pharmacology to mean a drug derived from opium. Opioid, a more modern term, is used to designate all substances, both natural and synthetic, that bind to opioid receptors (including antagonists). 
  3. Hemmings, Hugh C.; Egan, Talmage D. (2013). Pharmacology and Physiology for Anesthesia: Foundations and Clinical Application: Expert Consult - Online and Print. Elsevier Health Sciences. p. 253. ISBN 1437716792. Opiate is the older term classically used in pharmacology to mean a drug derived from opium. Opioid, a more modern term, is used to designate all substances, both natural and synthetic, that bind to opioid receptors (including antagonists). 
  4. Cammarano, W. B., Pittet, J. F., Weitz, S., Schlobohm, R. M., & Marks, J. D. (1998). Acute withdrawal syndrome related to the administration of analgesic and sedative medications in adult intensive care unit patients. Critical care medicine, 26(4), 676-684.
  5. The effect of opioid therapy on endocrine function. (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/23414717
  6. Opioid-induced androgen deficiency (OPIAD). (PubMed.gov / NCBI) | https://www.ncbi.nlm.nih.gov/pubmed/22786453
  7. Why Heroin Relapse Often Ends In Death - Lauren F Friedman (Business Insider) | http://www.businessinsider.com.au/philip-seymour-hoffman-overdose-2014-2
  8. Siegel, S., Hinson, R., Krank, M., & McCully, J. (1982). Heroin “overdose” death: contribution of drug-associated environmental cues. Science, 216(4544), 436–437. https://doi.org/10.1126/science.7200260