Nicotine is the critical reinforcing component responsible for most of the effects in humans.
α4β2- nicotinic acetylcholine receptors have reinforcing effects of nicotine, initially activate these receptors located on dopamine neurons in the ventral tegmental area; although rapidly desensitized, nicotine produces a sustained effect on dopamine release in the nucleus accumbens& this is critical to the drugs’ ability to induce motivational / reinforcing properties.
Although the nucleus accumbens plays a pivotal role in drug-seeking behaviour, the influence of prefrontal cortex, amygdala, hippocampus ( through glutamate / GABA neurons) mediate the drive to take drugs+ influence of drug-associated cues &the memory of drug taking.
Medications that act on glutamate or GABA systems hold the promise of reducing drug cravings or avoiding relapse.
Measures that limit the purchase of tobacco&exposure to tobacco smoke should be widely implemented/expanded to sustain the reduction of tobacco use.
Comprehensive effective tobacco control measures include increased taxation, consumer regulations, dissemination of information about tobacco products, legislation against advertising/ sponsorship by tobacco companies, economic alternatives to tobacco production / smoking cessation programs&warnings on cigarette packaging.
Individuals have also become particularly sensitive to environmental stimuli, or cues, that have acquired motivational salience through repeated associations with self-administered nicotine.
Tobacco-seeking, craving/relapse are well known to be triggered by these environmental stimuli.
The new regulations that restrict the use of tobacco in public places help to reduce the influence of these cues on behaviour &therefore help exsmokers to maintain their abstinence
Individuals are not at equal risk of tobacco dependence.
An important / significant genetic component play a role in several aspects of smoking behaviour, as the initiation/maintenance of smoking, the number of cigarettes smoked& the response to pharmacologic treatments.
A strong link exists between tobacco use & psychiatric disorders *2- 3, as schizophrenia, depression, drug addiction, suggests shared neurobiologic / behavioural abnormalities.
On the contrary tobacco may be used to improve the psychiatric condition or to reduce the side effects of some psychiatric medications,as tobacco smoke contains chemical substances other than nicotine that inhibit monoamine oxidase A/B in the brain mimic the effects of antidepressants, may explain the increased risk of depression for 6 months or longer following smoking cessation.
HCWs should systematically ask about tobacco use& advise the patient about the risks &about the availability of effective strategies to quit.
The next step is to assess the patient’s willingness to quit &if
not motivated, effective approaches (e.g., motivational interviewing) developed to enhance the patient’s motivation to quit.
For a patient who is motivated to quit, the goal of treatment is total abstinence, the only outcome associated with reduced health risks.
The use of pharmacologic trs as partial substitutes to reduce tobacco consumption &morbidity or mortality (harm reduction).
2 approaches proven effective for smoking cessation are pharmacotherapy / nonpharmacologic interventions&best results obtained when the 2 combined& pharmacotherapy increase chance of initiating / maintaining abstinence 23-fold& should be used more extensively.
Three distinct types : NRT, bupropion, varenicline.
Smokers with moderate to severe tobacco dependence respond best to these 3 types of pharmacotherapy& no consensus on which type should be used first, except on the basis of the preference & presence of contraindications.
Whichever chosen, it should be used first as monotherapy , since there is no clear evidence for additive effects of combining pharmacotherapies.
Combinations can be tested if monotherapy is not effective .
Combinations of various NRTs (e.g., patch ,gum, patch / inhaler) tested& NRT/ bupropion.
Other medications (nortriptyline,clonidine, selegiline, rimonabant) increase rates of smoking cessation significantly
Only nortriptyline/clonidine could be considered as second-line medications in patients who do not respond to first-line medications.
Several products;patch, gum, nasal spray, inhaler, tablet , lozenge.
No difference demonstrated between products.
Ineffectiveness is often due to improper use or insufficient dosage.
The dosage should be adjusted if there are clinical signs of toxic effects( nausea insomnia, palpitations) or of insufficient dosage (i.e. severe withdrawal symptoms as irritability, restlessness, anxiety, increased appetite, depressed mood).
If a patient finds one type ineffective or intolerable, it is useful to try another.
A nicotinic receptor partial agonist, acting like an agonist or an antagonist depending on the state of activation of nicotinic receptors.
Through its intrinsic partial activation of the α4β2-nicotinic acetylcholine recs, elicits a moderate/ sustained increase in mesolimbic dopamine& counteract the low dopamine encountered in the absence of nicotine during smoking cessation attempts.
By competitively binding to α4β2-nicotinic acetylcholine receps, as a partial agonist, protects against nicotine-induced dopaminergic activation if the patient smokes&disrupt the reinforcing effects of nicotine& compensate for withdrawal symptoms.
A significant effect on smoking cessation rates, higher than bupropion ,but no direct comparison with NRT conducted.
Varenicline efficacious in preventing smoking relapse.
Started at 0.5 mg once daily for the first 3 days, 0.5 mg twice daily for the next 4 days then 1 mg twice daily, for a total duration of 12-24 weeks (lower dosage in kidney disease or dialysis).
The main side effect of varenicline therapy is nausea,30%.
Majority of successful quits occur without direct medical assistance or without pharmacotherapy.
NPT are feasible & should be encouraged, especially by people for whom medication use is problematic, as adolescents/ pregnant.
Quitting attempts are encouraged by media or the quit advice.
Advising to quit, even just once, helps to double quit rates.
To initiate as many cessation attempts as possible, practitioners should advise all of their patients who smoke to quit.
Also, by using general motivational techniques or motivational enhancement therapy, the clinician promotes the patient’s self-motivational statements& the patient gains greater awareness of the problems associated with smoking.
During each patient contact, the clinician should ask about the person’s smoking status& provide information on available trts.
A variety of interventions efficacious, although may not be additive with pharmacologic interventions.
A more intensive approach, as behavioural cognitive therapy, can be useful to help patients recognize, avoid , cope with difficult situations most likely to initiate smoking.
Coping strategies also target maladaptive thoughts to prevent relapse.
Social support from their family, friends ,coworkers to establish a smoke-free home.
Increase their physical activity facilitate smoking cessation, most notably in women&limit the weight gain that frequently follows smoking cessation.
Most smokers will gain fewer than 5 kg after quitting, negligible compared with the risks associated with continued smoking.
Since smoking cessation is the priority, aggressive treatment to fight the weight gain (e.g strict dieting) are not recommended during a quit attempt,but once the patient has successfully quit smoking, dealt with later.