STIMULANTS: Nicotine predictable stages CSUF CSUF CSUF



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STIMULANTS: Nicotine (p.1) 1. History of Use mostly derived from the tobacco plant (Nicotiana tobacum) native to So. Amer., used by Mayans probably B.C. taken to Europe by Spanish explorers in 1500s returned to No. Amer. in 1600s (by British & others) where ever it was used, its use went through predictable stages: medicinal use & praise glamour/recreational use & faddism protest against its use (as unhealthy, unsafe, monetary fines) taxation, government control of access government continues to depend on revenue from taxation and does not outlaw tobacco access acceptance ( in bed with the devil!) history of use in USA: 1938 first study linking smoking to lung cancer 1954 relation between smoking & heart /lung disease noted 1964 Cigarette smoking may be hazardous to your health warning 1969 smoking permitted anywhere on CSUF campus, incl. classrooms 1970 Public Smoking Act (restricted smoking in some public places) 1971 tobacco ads banned on radio & TV 1971 Cigarette smoking is dangerous to your health warning *1995 smoking in CSUF classrooms banned (OK in hallways) *1979 smoking & non-smoking sections on domestic airlines *1981 smoking banned on all domestic flights within California *1985 smoking banned on all domestic flights within USA 1987 Surgeon General Koop issues warning nicotine is addicting *1991 smoking banned in California restaurants *1995 smoking banned in California bars 1994 FDA takes position that it should regulate cigarettes as a drug 1996 smoking banned in all major European airports *2000 smoking not permitted in CSUF buildings/balconies anywhere *approx. dates (subject to vagaries in my LTM)

STIMULANTS: Nicotine (p.2) 2. Demographics of Users (USA) the 3 most widely used psychoactive drugs are: caffeine, nicotine, ETOH 4K cigarettes/year/person 18 yrs. or older approximately 25% of population smokes cigarettes vs. 74-92% of schizophrenics! vs. an even higher % of alcoholics & persons Dx w/ depression! implications mean age of onset of smoking = 13 years implications 9 out of 10 smokers were addicted before the age of 21 years 6000 teens/day smoke their first cigarette 50% will go on to become habitual users 33% of these habitual users will eventually die of smoking-related causes approximately 2000 persons/day quit smoking but > 3000 persons/day start smoking thus, about a 2-3% yearly increase in smokers #s 34% of smokers try to quit smoking/year 2.5% succeed eventually about 50% of all smokers manage to quit proportion of adults who smoke as been decreasing (now about 25%, was 50% in 1965) smoking is directly responsible for about 1100 deaths/day while it is the nicotine which causes the dependence, it may be other ingredients (e.g. tars) that are the most toxic (e.g. cause cancer and cardiovascular damage)

STIMULANTS: Nicotine (p.3) 3. Pharmacokinetics Absorption: nicotine is water soluble and is readily absorbed if smoked, is an aerosol (liquid dispersed in a gas) absorbed into lungs, mucous membranes (chewed, inhaled as snuff) note: can be absorbed though skin (e.g. nicotine based insecticides) mean of 0.5 to 2.0 mg nicotine/cigarette absorb about 10-20% of that dose (0.05 to 0.4 mg/cigarette) into bloodstream 80-90% of original nicotine in cigarette goes off in uninhaled smoke but this uninhaled smoke can also be inhaled later by smoker in badly ventilated room or by a non-smoker in the vicinity 90% of nicotine in bloodstream passes BBB (0.045 to 0.36 mg), average of about 0.18 mg/cigarette with a latency of about 10 sec. also crosses placental barrier Metabolism & Elimination: nicotine is metabolized by liver enzyme CYP2A6 smoking induces liver enzymes (only if smoked) some SSRIs inhibit formation of CYP2A6 note: lower levels of CYP2A6 found in African Americans metabolized to cotinine ½ life is about 2 hours (in a chronic smoker) excretion is via the kidneys LD50 is 60 mg of nicotine

STIMULANTS: Nicotine (p.4) 4. Pharmacological Effects nicotine is a stimulant because it excites the CNS, but paradoxically it is felt as a calming agent (at lower dose levels, at least) note: in initial/early stages of smoking, nicotine produces very aversive effects: nausea, vomiting (is an irritant to GI tract) but tolerance develops quickly to this response nicotine --- attaches to ACh nicotinic RSs in PNS (somatic NS) initially --- stimulates the post-synaptic cell but as nicotine stays attached to RS, eventually becomes a RS blocker --- blocks cholinergic PNS RS --- muscle relaxation (at low doses) at high doses --- increased muscle activity (tremors, spasms) also stimulates preganglionic SNS RS (uses ACh) in PNS --- increased release of NE, E in postganglionic SNS neurons --- increased release of NE, E from adrenal medulla both of which --- increased BP, HR increased heart force peripheral vasoconstriction of cutaneous vessels vasodilation in skeletal muscle bloodvessels vasodilation in coronary arteries increased tendency to form blood clots increased motility in gut --- diarrhea initial increase in salivation, followed by decreased salivation & bronchial secretions increased respiratory rate (low doses) decreased respiratory rate (high doses)

STIMULANTS: Nicotine (p.5) 4. Pharmacological Effects (cont.) effects in CNS: increases the release of ADH (by hypothalamus) --- fluid retention increased CNS activity generally initially --- excitation, increased alertness, attention; followed by decreased CNS activity --- depression stimulation of area postrema (medulla) --- increased nausea/vomiting (followed by rapid tolerance) stimulation of medullary breathing centers and reduced O2 in bloodstream --- increased respiratory rate increased release of NE & DA in hypothalamus DA released in mesolimbic system, nucl. Accumbens, forebrain --- reinforcing effects, addiction, focus on nicotine (DA2 RSs) builds up tolerance --- increasing doses increased release of glutamate --- agitation, improved memory? increased release of 5HT --- sedation, decreased aggression general effects from CNS changes --- decreased appetite (& mild weight loss) increased motor activation, restlessness, figiting increased cognitive functioning improved sensory-motor performance (on simple tasks) increased memory consolidation (esp. STM vs. LTM) nicotine activates frontal lobes as an ACh agonist, may affect hippocampus, frontal lobes increased anxiety & panic attacks (via activation of cingulate gyrus & locus coeruleus, the latter structure related to control of vigilance, alertness, REM sleep, major source of ACh) nicotine may have an antidepressant effect implications there are many co-morbidities (dual Dxs) with smoking: conduct disorders, ADHD/ADD, depression smoking & adverse childhood events (divorce, mentally-ill parent, jailed parent, abuse, battering, etc.)

STIMULANTS: Nicotine (p.6) 5. Tolerance & Dependence does not show much biological tolerance to physiological effects although does develop tolerance to nausea/vomiting does develop tolerance to reinforcing effects --- increasing drug doses does develop dependence --- adverse withdrawal Sxs upon D/C drug thus, is adversive to D/C drug use of nicotine patches help with w/d effects (2x success rate) adverse w/d responses can last many months after D/Cd drug: irritability decreased concentration increased appetite anger restlessness weight gain anxiety impatience insomnia, fragmentation often increases use of caffeine when w/ding from nicotine 6. Toxicity acute toxicity (=> 10 mg): nausea cold disturbed vision salivation sweaty disturbed hearing abdominal pain headache mental confusion vomiting dizziness muscle weakness diarrhea faintness labored breathing hypotension irregular EKG weak/rapid pulse chronic toxicities: increased risk of cancer, esp. to lungs, bladder, mouth, tongue, etc. increased risk of pulmonary diseases (e.g. COPD, emphysema, asthma) increased risk of cardiovascular disease increased CO exposure --- heart muscle anoxia increased atherosclerosis (narrowed arteries) --- heart muscle anoxia increased risk of thrombosis (clotting, sticky platelets) above are all increased even more in pt. w/ dual diagnosis of diabetes summary increased risk of blockage of vital arteries to heart/brain

STIMULANTS: Nicotine (p.7) 6. Toxicity (cont.) and blockage of blood supply to rest of body areas/organs as well 450,000 persons die/year of smoking-related causes passive smoke inhalation also a major health risk 4,000 deaths/year due to lung cancer in non-smokers 37,000 deaths/year due to heart disease in non-smokers 7. Pregnancy & Reproduction nicotine reduces fertility & conception (interferes with fallopian cell cilia) increased risk of spontaneous abortions, stillborns increased risk of post-partum deaths increased risk of preterm deliveries decreased rates of intrauterine growth rates (up to 40%) increased low birth-weight babies (although normal by 1½ years) 2,000 infant deaths/year rel. to mother smoking fetal hypoxia (high CO levels, low O2 levels) increased risk of lowered IQ in child, increased risk of Dx of ADHD/ADD, & other behavioral problems later on (as damaged brain areas come on-line?) could mother smoking during pregnancy lead to changes in fetal RSs? greater risks for addictions, depression, conduct disorder, etc.? 8. Miscellaneous cigarette smoke is made up of 4,000+ compounds (from tobacco & paper) including CO, CO2, ammonia, cyanide, formaldehyde, nicotine, tars and others more than 43 known carcinogens with the 4,000+ smokers, esp. heavy smokers titrate their dose levels w/i a range

STIMULANTS: Nicotine (p.8) 9. Therapy for Nicotine Dependence quitting not easy success rates @ 6 months are 22-42% success rates of smoking cessation clinics is 12-28% of 41 million ex-smokers in USA, 90% quit on their own use nicotine replacement (w/ transdermal patches, gum, nasal sprays, inhalers) helps to slow down process of readjustment (up/down regulation of RSs, etc.) use DA/5HT/NE agonists to help reduce cravings Wellbutrin, Zyban (buproprion) this drug inhibits reuptake of DA & NE SEs includes increased risk of seizures note: naloxone increases cravings implies endogenous opioids involved somehow use antidepressants (e.g. SSRI) if depression is also present support groups, behavioral charting, cognitive therapy, etc. e.g. avoiding triggers (e.g. coffee, ETOH, driving) 10. Is nicotine good for anything?... Yes! a pesticide/insecticide smoking correlated with lowered risk of PD & Alzheimer s disease