Toxicomanie

Toxicomania sau Narcomania este dependența unor persoane dependente de substanțe stupefiante. Persoanele care suferă de asemenea deranjamente se numesc toxicomani sau narcomani. Există denumiri specifice pentru dependența de anumite substanțe determinate.

Dependența de substanțe, cunoscută și sub numele de dependență de droguri, este o stare adaptivă care se dezvoltă din administrarea repetată a drogului și care are ca rezultat sevrajul la încetarea consumului de droguri.^[1]^[2] O dependență de droguri, un concept distinct față de dependența de substanțe, este definită ca o utilizare compulsivă, în afara controlului, în ciuda consecințelor negative.^[1]^[2] Un medicament dependent este un medicament care este atât recompensarea, cât și consolidarea.^[1] DeltaFosB, un factor de transcriere a genei, este acum cunoscut ca fiind o componentă critică și un factor comun în dezvoltarea practic a tuturor formelor obișnuințe comportamentale și de droguri,^[3]^[4]^[5] dar nu dependență.

Cele mai populare substanțe în toxicomanie modificare

Medicamente care conțin toluen modificare

Deoarece toluenul în forma sa pură este interzis, este destul de greu să-l cumperi la vânzare, deci substanțele toxice utilizează substanțe care conțin toluol: acestea pot fi diferite branduri de adezivi, lacuri și solvenți care sunt inhalate prin ambalaj. În funcție de concentrația de toluen, efectul halucinogen are loc cu o durată diferită de inhalare.

Benzine modificare

În ciuda creșterii costului benzinei, acesta este încă mult mai mic decât prețul acelorași solvenți, dar efectul său este aproximativ același cu cel al substanțelor care conțin toluol. Vaporii de benzină sunt consumați nu numai prin saci, ci și prin sticle de plastic.

Gaz de uz casnic modificare

Principala sursă de gaze naturale sunt cilindrii pentru umplerea brichetelor, precum și a brichetelor. Inhalarea gazelor se face prin prinderea supapei cilindrului combinată cu o respirație profundă cu dinții. După câteva respirații profunde, halucinațiile apar pentru câteva minute. În viitor, acest lucru se poate repeta. Abuzul de gaze sau substanțe (în mod obișnuit "sniffing") este cel mai periculos tip de abuz de substanțe. Gazul nu lasă în urmă un miros, nu are un gust atât de urât și se volatilizează ușor. Dar, în același timp, poate provoca asfixierea datorată umplerii plămânilor și deplasarea oxigenului și pierderea conștiinței cu un rezultat fatal. Este tocmai asfixierea datorată excluderii aerului din plămâni, care este cea mai frecventă cauză de deces al dependenților de gaz. Merită să ne amintim că pentru a calcula doza halucinogenă și letală de gaz este aproape imposibilă.

Nu uitati ca durata medie de viata a unui dependent sistemic inveterate rar depaseste 2 ani de la data inceperii utilizarii regulate a produselor chimice de uz casnic in alte scopuri. Există, de asemenea, un mit despre utilizarea acetonului de către dependenți. Acetona nu este halucinogenă sau intoxicantă și nu este utilizată în abuzul de substanțe.

Toxicomania pasivă modificare

Abuzul de substanțe abuzive este un fenomen în care victima otrăvirii chimice nu intenționează să utilizeze nici o substanță chimică, dar în procesul de lucru (de exemplu, renovarea apartamentului, mobilierul sau fabricarea anumitor produse) respiră în fumul acelor substanțe, ceea ce poate duce la intoxicații toxice și halucinații. Cel mai adesea acest lucru are loc într-un spațiu închis. Măștile de gaz, respiratoarele și ventilația sunt folosite pentru a combate acest lucru, dar se întâmplă adesea ca anumite condiții să nu permită respectarea măsurilor de siguranță atunci când folosesc astfel de substanțe. Au fost de asemenea multe cazuri când, după utilizarea materialelor de finisare de calitate slabă, ca material de vopsea de alt scop, spațiul închis a devenit literalmente o cameră de gazare. Aceasta înseamnă că o persoană care trăiește sau lucrează în astfel de spații poate să nu observe pentru sine că devine abuzator de substanțe.

Note modificare

^ ^a ^b ^c Malenka RC, Nestler EJ, Hyman SE (2009). „Chapter 15: Reinforcement and Addictive Disorders”. În Sydor A, Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (ed. 2nd). New York: McGraw-Hill Medical. pp. 364–368. ISBN 9780071481274. The defining feature of addiction is compulsive, out-of-control drug use, despite negative consequences. ...
Addictive drugs are both rewarding and reinforcing. ... Familiar pharmacologic terms such as tolerance, dependence, and sensitization are useful in describing some of the time-dependent processes that underlie addiction. ...
Dependence is defined as an adaptive state that develops in response to repeated drug administration, and is unmasked during withdrawal, which occurs when drug taking stops. Dependence from long-term drug use may have both a somatic component, manifested by physical symptoms, and an emotional–motivation component, manifested by dysphoria. While physical dependence and withdrawal occur with some drugs of abuse (opiates, ethanol), these phenomena are not useful in the diagnosis of addiction because they do not occur with other drugs of abuse (cocaine, amphetamine) and can occur with many drugs that are not abused (propranolol, clonidine).

The official diagnosis of drug addiction by the Diagnostic and Statistic Manual of Mental Disorders (2000), which makes distinctions between drug use, abuse, and substance dependence, is flawed. First, diagnosis of drug use versus abuse can be arbitrary and reflect cultural norms, not medical phenomena. Second, the term substance dependence implies that dependence is the primary pharmacologic phenomenon underlying addiction, which is likely not true, as tolerance, sensitization, and learning and memory also play central roles. It is ironic and unfortunate that the Manual avoids use of the term addiction, which provides the best description of the clinical syndrome.
^ ^a ^b „Substance use disorder”. Pubmed Health. National Institutes of Health. Arhivat din originalul de la 31 martie 2014. Accesat în 12 septembrie 2014. Drug dependence means that a person needs a drug to function normally. Abruptly stopping the drug leads to withdrawal symptoms. Drug addiction is the compulsive use of a substance, despite its negative or dangerous effects
^ Robison AJ, Nestler EJ (octombrie 2011). „Transcriptional and epigenetic mechanisms of addiction”. Nature Reviews. Neuroscience. 12 (11): 623–37. doi:10.1038/nrn3111. PMC 3272277  . PMID 21989194. ΔFosB has been linked directly to several addiction-related behaviors ... Importantly, genetic or viral overexpression of ΔJunD, a dominant negative mutant of JunD which antagonizes ΔFosB- and other AP-1-mediated transcriptional activity, in the NAc or OFC blocks these key effects of drug exposure14,22–24. This indicates that ΔFosB is both necessary and sufficient for many of the changes wrought in the brain by chronic drug exposure. ΔFosB is also induced in D1-type NAc MSNs by chronic consumption of several natural rewards, including sucrose, high fat food, sex, wheel running, where it promotes that consumption14,26–30. This implicates ΔFosB in the regulation of natural rewards under normal conditions and perhaps during pathological addictive-like states.
^ Blum K, Werner T, Carnes S, Carnes P, Bowirrat A, Giordano J, Oscar-Berman M, Gold M (2012). „Sex, drugs, and rock 'n' roll: hypothesizing common mesolimbic activation as a function of reward gene polymorphisms”. Journal of Psychoactive Drugs. 44 (1): 38–55. doi:10.1080/02791072.2012.662112. PMC 4040958  . PMID 22641964. It has been found that deltaFosB gene in the NAc is critical for reinforcing effects of sexual reward. Pitchers and colleagues (2010) reported that sexual experience was shown to cause DeltaFosB accumulation in several limbic brain regions including the NAc, medial pre-frontal cortex, VTA, caudate, and putamen, but not the medial preoptic nucleus. Next, the induction of c-Fos, a downstream (repressed) target of DeltaFosB, was measured in sexually experienced and naive animals. The number of mating-induced c-Fos-IR cells was significantly decreased in sexually experienced animals compared to sexually naive controls. Finally, DeltaFosB levels and its activity in the NAc were manipulated using viral-mediated gene transfer to study its potential role in mediating sexual experience and experience-induced facilitation of sexual performance. Animals with DeltaFosB overexpression displayed enhanced facilitation of sexual performance with sexual experience relative to controls. In contrast, the expression of DeltaJunD, a dominant-negative binding partner of DeltaFosB, attenuated sexual experience-induced facilitation of sexual performance, and stunted long-term maintenance of facilitation compared to DeltaFosB overexpressing group. Together, these findings support a critical role for DeltaFosB expression in the NAc in the reinforcing effects of sexual behavior and sexual experience-induced facilitation of sexual performance. ... both drug addiction and sexual addiction represent pathological forms of neuroplasticity along with the emergence of aberrant behaviors involving a cascade of neurochemical changes mainly in the brain's rewarding circuitry.
^ Olsen CM (decembrie 2011). „Natural rewards, neuroplasticity, and non-drug addictions”. Neuropharmacology. 61 (7): 1109–22. doi:10.1016/j.neuropharm.2011.03.010. PMC 3139704  . PMID 21459101.

Legături externe modificare

Portalul Sănătate-UE - Droguri

[NHM_terms-DSM_flaw-1] Malenka RC, Nestler EJ, Hyman SE (2009). „Chapter 15: Reinforcement and Addictive Disorders”. În Sydor A, Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (ed. 2nd). New York: McGraw-Hill Medical. pp. 364–368. ISBN 9780071481274. The defining feature of addiction is compulsive, out-of-control drug use, despite negative consequences. ...
Addictive drugs are both rewarding and reinforcing. ... Familiar pharmacologic terms such as tolerance, dependence, and sensitization are useful in describing some of the time-dependent processes that underlie addiction. ...
Dependence is defined as an adaptive state that develops in response to repeated drug administration, and is unmasked during withdrawal, which occurs when drug taking stops. Dependence from long-term drug use may have both a somatic component, manifested by physical symptoms, and an emotional–motivation component, manifested by dysphoria. While physical dependence and withdrawal occur with some drugs of abuse (opiates, ethanol), these phenomena are not useful in the diagnosis of addiction because they do not occur with other drugs of abuse (cocaine, amphetamine) and can occur with many drugs that are not abused (propranolol, clonidine).

The official diagnosis of drug addiction by the Diagnostic and Statistic Manual of Mental Disorders (2000), which makes distinctions between drug use, abuse, and substance dependence, is flawed. First, diagnosis of drug use versus abuse can be arbitrary and reflect cultural norms, not medical phenomena. Second, the term substance dependence implies that dependence is the primary pharmacologic phenomenon underlying addiction, which is likely not true, as tolerance, sensitization, and learning and memory also play central roles. It is ironic and unfortunate that the Manual avoids use of the term addiction, which provides the best description of the clinical syndrome.

[NIH-2] „Substance use disorder”. Pubmed Health. National Institutes of Health. Arhivat din originalul de la 31 martie 2014. Accesat în 12 septembrie 2014. Drug dependence means that a person needs a drug to function normally. Abruptly stopping the drug leads to withdrawal symptoms. Drug addiction is the compulsive use of a substance, despite its negative or dangerous effects

[Nestler-3] Robison AJ, Nestler EJ (octombrie 2011). „Transcriptional and epigenetic mechanisms of addiction”. Nature Reviews. Neuroscience. 12 (11): 623–37. doi:10.1038/nrn3111. PMC 3272277  . PMID 21989194. ΔFosB has been linked directly to several addiction-related behaviors ... Importantly, genetic or viral overexpression of ΔJunD, a dominant negative mutant of JunD which antagonizes ΔFosB- and other AP-1-mediated transcriptional activity, in the NAc or OFC blocks these key effects of drug exposure14,22–24. This indicates that ΔFosB is both necessary and sufficient for many of the changes wrought in the brain by chronic drug exposure. ΔFosB is also induced in D1-type NAc MSNs by chronic consumption of several natural rewards, including sucrose, high fat food, sex, wheel running, where it promotes that consumption14,26–30. This implicates ΔFosB in the regulation of natural rewards under normal conditions and perhaps during pathological addictive-like states.

[ΔFosB_reward-4] Blum K, Werner T, Carnes S, Carnes P, Bowirrat A, Giordano J, Oscar-Berman M, Gold M (2012). „Sex, drugs, and rock 'n' roll: hypothesizing common mesolimbic activation as a function of reward gene polymorphisms”. Journal of Psychoactive Drugs. 44 (1): 38–55. doi:10.1080/02791072.2012.662112. PMC 4040958  . PMID 22641964. It has been found that deltaFosB gene in the NAc is critical for reinforcing effects of sexual reward. Pitchers and colleagues (2010) reported that sexual experience was shown to cause DeltaFosB accumulation in several limbic brain regions including the NAc, medial pre-frontal cortex, VTA, caudate, and putamen, but not the medial preoptic nucleus. Next, the induction of c-Fos, a downstream (repressed) target of DeltaFosB, was measured in sexually experienced and naive animals. The number of mating-induced c-Fos-IR cells was significantly decreased in sexually experienced animals compared to sexually naive controls. Finally, DeltaFosB levels and its activity in the NAc were manipulated using viral-mediated gene transfer to study its potential role in mediating sexual experience and experience-induced facilitation of sexual performance. Animals with DeltaFosB overexpression displayed enhanced facilitation of sexual performance with sexual experience relative to controls. In contrast, the expression of DeltaJunD, a dominant-negative binding partner of DeltaFosB, attenuated sexual experience-induced facilitation of sexual performance, and stunted long-term maintenance of facilitation compared to DeltaFosB overexpressing group. Together, these findings support a critical role for DeltaFosB expression in the NAc in the reinforcing effects of sexual behavior and sexual experience-induced facilitation of sexual performance. ... both drug addiction and sexual addiction represent pathological forms of neuroplasticity along with the emergence of aberrant behaviors involving a cascade of neurochemical changes mainly in the brain's rewarding circuitry.

[Natural_and_drug_addictions-5] Olsen CM (decembrie 2011). „Natural rewards, neuroplasticity, and non-drug addictions”. Neuropharmacology. 61 (7): 1109–22. doi:10.1016/j.neuropharm.2011.03.010. PMC 3139704  . PMID 21459101.

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