Qaramlik – sezilarli zarar va salbiy oqibatlarga qaramay, giyohvand moddalarni (shu jumladan spirtli ichimliklarni) doimiy ravishda iste’mol qilish bilan tavsiflanadigan biopsixosotsial kasallik
Giyohvandlik vositasi – qayta-qayta iste’mol qilinganda giyohvand moddalarni iste’mol qilish buzilishining sezilarli darajada yuqori ko‘rsatkichlari bilan bog‘liq bo‘lgan psixoaktiv moddalar, asosan giyohvand moddaning miyaga ta’siri bilan bog‘liq reward systems
tobelik – stimulning takroriy ta’siri to‘xtatilganda (masalan, dori-darmonlarni qabul qilish) abstinent sindrom bilan bog‘liq bo‘lgan moslashish holati
giyohvand moddalarga moslashish yoki teskari tolerantlik – ma’lum bir dozada dori vositasining takroran qo‘llanilishi natijasida uning ta’sirining kuchayib borishi
Ushbu adnozada quyidagi havolalardan ushbu atamalarning taʼriflari ishlatiladi (eslatma: ular qisqaroq bo‘lishi uchun biroz o‘zgartirilgan):
Andoza manbalar roʻyxati; kengaytirish uchun o‘ng tomondagi koʻrsatish tugmasini bosing →
Manbalar
↑ „Chapter 15: Reinforcement and Addictive Disorders“, Molecular Neuropharmacology: A Foundation for Clinical Neuroscience, 2nd, New York: McGraw-Hill Medical, 2009 — 364–375-bet. ISBN 9780071481274.
↑Nestler EJ (December 2013). "Cellular basis of memory for addiction". Dialogues in Clinical Neuroscience15 (4): 431–443. PMID24459410. PMC3898681. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=3898681. "Despite the importance of numerous psychosocial factors, at its core, drug addiction involves a biological process: the ability of repeated exposure to a drug of abuse to induce changes in a vulnerable brain that drive the compulsive seeking and taking of drugs, and loss of control over drug use, that define a state of addiction. ... A large body of literature has demonstrated that such ΔFosB induction in D1-type [nucleus accumbens] neurons increases an animal's sensitivity to drug as well as natural rewards and promotes drug self-administration, presumably through a process of positive reinforcement ... Another ΔFosB target is cFos: as ΔFosB accumulates with repeated drug exposure it represses c-Fos and contributes to the molecular switch whereby ΔFosB is selectively induced in the chronic drug-treated state.41. ... Moreover, there is increasing evidence that, despite a range of genetic risks for addiction across the population, exposure to sufficiently high doses of a drug for long periods of time can transform someone who has relatively lower genetic loading into an addict."
↑"Neurobiologic Advances from the Brain Disease Model of Addiction". New England Journal of Medicine374 (4): 363–371. January 2016. doi:10.1056/NEJMra1511480. PMID26816013. PMC6135257. //www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=6135257. "Substance-use disorder: A diagnostic term in the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5) referring to recurrent use of alcohol or other drugs that causes clinically and functionally significant impairment, such as health problems, disability, and failure to meet major responsibilities at work, school, or home. Depending on the level of severity, this disorder is classified as mild, moderate, or severe. Addiction: A term used to indicate the most severe, chronic stage of substance-use disorder, in which there is a substantial loss of self-control, as indicated by compulsive drug taking despite the desire to stop taking the drug. In the DSM-5, the term addiction is synonymous with the classification of severe substance-use disorder."
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