Smoking pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Aravind Kuchkuntla, M.B.B.S[2]
Overview
Nicotine from the cigarette is rapidly absorbed form the lungs and diffuses readily into brain where it binds to nicotinic acetylcholine receptors. Stimulation of nicotinic acetyl choline receptor in the brain results in the release dopamine and other neurotransmitters which are responsible for the feeling of pleasure.
Pathophysiology
Pathogenesis
- Nicotine is the primary addictive substance in tobacco.
- Nicotine from the cigarette is rapidly absorbed form the lungs and diffuses readily into brain where it binds to nicotinic acetylcholine receptors.[1]
- Nicotine exists in charged and uncharged forms in the blood stream. The uncharged form diffuses directly into the lipid membranes and the charged form attaches to the nicotine receptors.[2]
- The nicotinic acetyl choline receptor is a ligand gated channel complex composed of five subunits which are present in abundance in the brain. These receptors subtypes are believed play a role in mediating nicotine dependence.
- Stimulation of nicotinic acetyl choline receptor in the brain results in the release dopamine and other neurotransmitters which are responsible for the feeling of pleasure.[3]
- Chronic exposure of the brain to nicotine results in adaptation and needing increased demands of nicotine for the brain to function normally. Therefore, cessation of smoking abruptly causes withdrawal symptoms of irritability, anxiety, problems getting along with others, difficulty concentrating, hunger, and weight gain.[4]
- Nicotine addiction is sustained by positive effects of pleasure and arousal and to avoid the adverse effects of nicotine withdrawal.
Genetics
- CYP2A6 gene codes for the enzymes metabolizing nicotine. Polymorphisms in the gene can result in the variability in individual smoking response and addictive behavior by influencing the nicotine metabolism in the body .[5]
References
- ↑ Prochaska JJ, Benowitz NL (2016). "The Past, Present, and Future of Nicotine Addiction Therapy". Annu Rev Med. 67: 467–86. doi:10.1146/annurev-med-111314-033712. PMC 5117107. PMID 26332005.
- ↑ Benowitz NL, Hukkanen J, Jacob P (2009). "Nicotine chemistry, metabolism, kinetics and biomarkers". Handb Exp Pharmacol (192): 29–60. doi:10.1007/978-3-540-69248-5_2. PMC 2953858. PMID 19184645.
- ↑ Subramaniyan M, Dani JA (2015). "Dopaminergic and cholinergic learning mechanisms in nicotine addiction". Ann N Y Acad Sci. 1349: 46–63. doi:10.1111/nyas.12871. PMC 4564314. PMID 26301866.
- ↑ Benowitz NL (2010). "Nicotine addiction". N Engl J Med. 362 (24): 2295–303. doi:10.1056/NEJMra0809890. PMC 2928221. PMID 20554984.
- ↑ López-Flores LA, Pérez-Rubio G, Falfán-Valencia R (2017). "Distribution of polymorphic variants of CYP2A6 and their involvement in nicotine addiction". EXCLI J. 16: 174–196. doi:10.17179/excli2016-847. PMC 5427481. PMID 28507465.