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Cigarette smoking is the single most preventable cause of premature
death in the United States. Smoking harms nearly every organ of the
body, causing many diseases (including, but not limited to,
cardiovascular disease, pulmonary disease, and cancers) and reducing
the health of smokers in general. Quitting smoking has immediate as
well as long-term benefits, reducing risks for diseases caused by
smoking and improving health in general.
Tobacco products are effective delivery systems for the drug nicotine.
Nicotine is a highly addictive drug that activates the dopamine reward
pathway in the brain that reinforces continued tobacco use. Nicotine
withdrawalsymptoms (e.g., irritability, anxiety, difficulty concentrating,
restlessness, depressed mood, insomnia, impaired performance,
increased appetite or weight gain, cravings) generally occur when
Constituents in tobacco smoke are associated with a number of clinically
significant drug interactions.
Tobacco dependence, a chronic disease that often requires repeated
intervention and multiple attempts to quit, is characterized by physiologic
dependence (addiction to nicotine) and behavioral habit of using
Numerous effective medications, as delineated in the Clinical Practice
Guideline, are available for treating tobacco use and dependence. Most
patients should be encouraged to use one or more first-line agents,
which include the nicotine patch, nicotine gum, nicotine lozenge, nicotine
nasalspray, nicotine oral inhaler, sustained-release bupropion, and
varenicline. All first-line agents approximately double quit rates, and
therefore, the choice of therapy is based largely on contraindications,
precautions, patient preference, and tolerability. In some cases,
medications can be combined or used for extended durations. Although
alternative therapies are available, these are not recommended because
of insufficient evidence of efficacy.
Comprehensive counseling, as defined by the Clinical Practice Guideline,
includes asking about tobacco use, advising patients to quit, assessing
readiness to quit, assisting patients with quitting, and arranging followCase 91-1 (Questions 2, 5),
up. This approach is referred to as “The 5 A’s.” Counseling and support
can be provided a variety of ways, such as through individual
counseling, group programs, telephone, or the Internet. Two components
of counseling are especially effective and should be applied when
assisting patients with quitting: practical counseling (problem solving or
skills training) and socialsupport delivered as part of treatment. Relapse
is common, and clinicians should work with patients throughout the quit
attempt to increase the chances for long-term abstinence.
Brief tobacco dependence treatment (<3 minutes) is effective. In the
absence of time or expertise, ask about tobacco use, advise patients to
is referred to as “Ask-Advise-Refer.”
Patients with psychiatric disorders exhibit a higher prevalence of tobacco
use and a disproportionately high level of tobacco-related morbidity and
Cigarettes are the most common form of tobacco used in the United
States; however, other forms of tobacco exist (spit tobacco, pipes,
cigars, bidis, hookah). All forms of tobacco are harmful.
Tobacco is a detrimental substance, and its use dramatically increases a person’s
odds of dependence, disease, disability, and death. Cigarettes are the only marketed
consumable product that when used as intended will contribute to the death of half or
1 Tobacco products are carefully engineered formulations that
optimize the delivery of nicotine, a chemical that meets the criteria for an addictive
substance: (a) nicotine induces psychoactive effects, (b) it is used in a highly
controlled or compulsive manner, and (c) behavioral patterns of tobacco use are
reinforced by the pharmacologic effects of nicotine.
2 As a major risk factor for a
wide range of diseases, including cardiovascular conditions, cancers, and pulmonary
disorders, tobacco is the primary known preventable cause of premature death and
3 Since the Surgeon General’s first report on smoking in 1964,
over 20 million American deaths have been attributed to smoking or secondhand
3 Globally, almost 7 million people die annually from smoking (6
million) or being exposed to secondhand smoke (890,000).
In the United States, smoking is responsible for more than 480,000 premature
In addition to the harm imposed on users of tobacco, exposure to
secondhand smoke results in an estimated 50,000 deaths annually.
Office of the US Surgeon General, there is no risk-free level of exposure to tobacco
2 Because of the health and societal burdens that it imposes, tobacco use and
dependence should be addressed during each clinical encounter with all tobacco
EPIDEMIOLOGY OF TOBACCO USE AND
In the United States, cigarettes are the most common form of tobacco that is
consumed, but other forms are also prevalent: smokeless tobacco (chewing tobacco,
oral snuff), pipes, cigars, clove cigarettes, bidis, and hookah. Electronic cigarettes
(e-cigarettes) are growing in popularity. Electronic cigarettes, electronic nicotine
delivery systems (ENDS), contain a liquid consisting of nicotine and other
substances that is heated by an atomizer and inhaled as a vapor. Among adults,
smoking prevalence varies by sociodemographic factors, including sex, race or
ethnicity, education level, age, and poverty level. The Centers for Disease Control
and Prevention (CDC) reported that in 2014, 21.3% of adults in the United States
used a tobacco product every day or some days, with 17% reporting cigarette use.
Factors Contributing to Tobacco Use
Tobacco addiction is maintained by nicotine dependence.
variety of pharmacologic effects that lead to dependence.
dependence is not simply a matter of nicotine pharmacology—it is a result of the
interplay of complex processes, including the desire for the direct pharmacologic
actions of nicotine, the relief of withdrawal, learned associations, and environmental
cues (e.g., advertising, the smell of a cigarette, or observing others who are
11 Physiologic factors, such as preexisting medical conditions (e.g.,
9,11 and one’s genetic profile), also can predispose
Nicotine, the addictive component of tobacco, is rapidly absorbed and passes
through the blood–brain barrier, contributing to its addictive nature. After inhalation,
nicotine reaches the brain within seconds.
10 As such, smokers experience nearly
immediate onset of the positive effects of nicotine, including pleasure, relief of
anxiety, improved task performance, improved memory, mood modulation, and
10 These effects, mediated by alterations in
neurotransmitter levels, reinforce continued use of nicotine-containing products.
Nicotine (Nicotiana tabacum) is one of the few natural alkaloids that exist in the
liquid state. Nicotine is a clear, weak base with a pKα of 8.0.
nicotine is ionized and poorly absorbed; conversely, in alkaline media, nicotine is
nonionized and well absorbed. Under physiologic conditions (pH = 7.4), a large
proportion of nicotine is nonionized and readily crosses cell membranes.
relation between pH and absorption, the tobacco industry and pharmaceutical
companies are able to titrate the pH of their tobacco products and nicotine
replacement therapy (NRT) products to maximize the absorption potential of
Once absorbed, nicotine induces a variety of central nervous system,
cardiovascular, and metabolic effects. Nicotine stimulates the release of several
neurotransmitters, inducing a range of pharmacologic effects such as pleasure
(dopamine), arousal (acetylcholine, norepinephrine), cognitive enhancement
(acetylcholine), appetite suppression (dopamine, norepinephrine, serotonin), learning
(glutamate), memory enhancement (glutamate), mood modulation (serotonin), and
reduction of anxiety and tension (β-endorphin and γ-aminobutyric acid [GABA]).
The dopamine reward pathway, a network that elicits feelings of pleasure in
response to certain stimuli, is central to drug-induced reward. The neurons of the
ventral tegmental area contain the neurotransmitter dopamine, which is released in
the nucleus accumbens and in the prefrontal cortex. Immediately after inhalation, a
bolus of nicotine enters the brain, stimulating the release of dopamine, which induces
nearly immediate feelings of pleasure, along with relief of the symptoms of nicotine
withdrawal. This rapid dose response reinforces repeated administration of the drug
and perpetuates the smoking behavior.
Chronic administration of nicotine has been shown to increase the number of
nicotine receptors in specific regions of the brain.
18 This may represent upregulation
in response to nicotine-mediated desensitization of the receptors and could play a
role in nicotine tolerance and dependence.
17,18 Chronic nicotine administration also
leads to tolerance of its behavioral and cardiovascular effects during the course of
the day; however, tobacco users regain sensitivity to the effects of nicotine after
overnight abstinence from nicotine,
10,11 as shown in Figure 91-1.
first cigarette of the day, the smoker experiences marked pharmacologic effects,
particularly arousal. No other cigarette throughout the day produces the same degree
of pleasure or arousal. For this reason, many smokers describe the first cigarette as
the most important one of the day. Shortly after the initial cigarette, tolerance begins
to develop. Accordingly, the threshold levels for both pleasure or arousal and
abstinence rise progressively throughout the day because the smoker becomes
tolerant to the effects of nicotine. With continued smoking, nicotine accumulates,
leading to an even greater degree of tolerance. Later in the day, each individual
cigarette produces only limited pleasure or arousal; instead, smoking primarily
alleviates nicotine withdrawal symptoms. Lack of exposure to nicotine overnight
results in resensitization of drug responses (i.e., loss of tolerance). Most dependent
smokers tend to smoke a certain number of cigarettes/day and tend to consume
sufficient nicotine/day to achieve the desired effects of cigarette smoking and
minimize the symptoms of nicotine withdrawal.
11,19 Withdrawal symptoms, which
include anger, anxiety, depression, difficulty concentrating, impatience, insomnia,
and restlessness, typically manifest within a few days after quitting, peak within a
week, and subside within 2 to 4 weeks.
20 Tobacco users become adept at titrating
their nicotine levels throughout the day to avoid withdrawal symptoms, maintain
pleasure and arousal, and modulate mood.
Figure 91-1 Nicotine addiction cycle throughout the day. The sawtooth line represents venous plasma
Benowitz NL. Cigarette smoking and nicotine addiction. Med Clin North Am. 1992;76(2):415.)
Nicotine is extensively metabolized in the liver and, to a lesser extent, in the
kidney and lung. Approximately 70% to 80% of nicotine is metabolized to cotinine,
14 The rapid metabolism of nicotine (half-life [t1/2
to inactive compounds underlies tobacco users’ needs for frequent, repeated
administration. The half-life of cotinine, however, is much longer (t1/2 = 18–20
hours), and for this reason, cotinine is commonly used as a marker of tobacco use as
well as a marker for exposure to secondhand smoke.
cannot, however, differentiate between the nicotine from tobacco products and the
nicotine from NRT products. Nicotine and other metabolites are excreted in the urine.
Urinary excretion is pH dependent; the excretion rate is increased in acidic urine.
Nicotine crosses the placenta and accumulates in breast milk.
Drug Interactions with Smoking
It is widely recognized that polycyclic aromatic hydrocarbons (PAHs) in tobacco
smoke are responsible for most drug interactions with smoking.
result from incomplete combustion of tobacco, are potent inducers of several hepatic
cytochrome-P450 microsomal enzymes (CYP1A1, CYP1A2, and possibly CYP2E1).
Although other substances in tobacco smoke, including acetone, pyridines, benzene,
nicotine, carbon monoxide, and heavy metals (e.g., cadmium), might also interact
with hepatic enzymes, their effects appear to be less significant. Most drug
interactions with tobacco smoke are pharmacokinetic, resulting from the induction of
drug-metabolizing enzymes (especially CYP1A2) by compounds in tobacco smoke.
Table 91-1 summarizes key interactions with smoking.
smoking, quit smoking, or dramatically alter their level of smoking might require
dosage adjustments for some medications.
Health Consequences of Tobacco Use
All forms of tobacco are harmful, and there is no safe level of exposure to tobacco
products. Smoking has a causal or contributory role in the development of a variety
of medical conditions, affecting almost every organ in the body.
Exposure to secondhand smoke, which includes the smoke from burning tobacco and
that exhaled by the smoker, affects an estimated 88 million nonsmokers older than the
age of 3 in the United States.
24 Secondhand smoke exposure causes disease and
premature death in children and adults who do not smoke resulting in an estimated
6 Millions of American children and adults are still exposed
to secondhand smoke in their homes and workplaces despite substantial progress in
tobacco control. Evidence indicates that there is no risk-free level of exposure to
secondhand smoke. Only completely eliminating smoking in indoor spaces fully
protects nonsmokers from exposure to secondhand smoke. Separating smokers from
nonsmokers, cleaning the air, and ventilating buildings cannot eliminate exposure of
nonsmokers to secondhand smoke.
Benefits of smoking cessation incurred soon after quitting (e.g., within 2 weeks–3
months) include improvements in pulmonary function, circulation, and ambulation.
Smoking cessation results in measurable improvements in lung function (see Chapter
19, Chronic Obstructive Pulmonary Disease). One year after cessation, the excess
risk of coronary heart disease is reduced to half that of continuing smokers. After 5 to
15 years, the risk of stroke is reduced to a rate similar to that of people who are
lifetime nonsmokers, and 10 years after quitting, the chance of dying of lung cancer is
approximately half that of continuing smokers. In addition, the risk of developing
mouth, throat, esophagus, bladder, kidney, or pancreatic cancer is decreased. Finally,
15 years after quitting, the risk of coronary heart disease is reduced to a rate that is
similar to that of people who have never smoked.
25 Similarly, more recent data
suggest that smokers who quit for good over a sustained period have an overall
mortality rate and death rate associated with cardiovascular disease, ischemic heart
disease, and stroke that is similar to individuals who have never smoked. In contrast,
individuals who had successfully quit, but later resumed smoking, had mortality risks
that were significantly higher than lifetime nonsmokers.
Drug Interactions with Tobacco Smoke
Drug/Class Mechanism of Interaction and Effects
Metabolized by CYP1A2. Manufacturer recommends using with caution in
smokers due to likely ↓ bendamustine concentrations, with ↑
concentrations of its two active metabolites.
Caffeine ↑ Metabolism (induction of CYP1A2); ↑ clearance (56%).
Caffeine levels likely increase after cessation.
↓ AUC (36%) and serum concentrations (24%).
↓ Sedation and hypotension possible in smokers; smokers may require ↑ dosages.
Clopidogrel (Plavix) ↑ Metabolism (induction of CYP1A2) of clopidogrel to its active
Clopidogrel’s effects are enhanced in smokers (≥10 cigarettes/day):
significant ↑ platelet inhibition, ↓ platelet aggregation; although
improved clinical outcomes have been shown, may also ↑ risk of
Clozapine (Clozaril) ↑ Metabolism (induction of CYP1A2); ↓ plasma concentrations (18%).
↑ Levels on cessation may occur; closely monitor drug levels and reduce
dose as required to avoid toxicity.
Erlotinib (Tarceva) ↑ Clearance (24%); ↓ trough serum concentrations (2-fold).
Flecainide (Tambocor) ↑ Clearance (61%); ↓ trough serum concentrations (25%).
Fluvoxamine (Luvox) ↑ Metabolism (induction of CYP1A2); ↑ clearance (24%); ↓ AUC (31%); ↓
Dosage modifications not routinely recommended but smokers may need
Haloperidol (Haldol) ↑ Clearance (44%); ↓ serum concentrations (70%); data are inconsistent
therefore clinical significance is unclear.
Heparin Mechanism unknown but ↑ clearance and ↓ half-life are observed. Smoking has
Smokers may need ↑ dosages because of PK and PD interactions.
may cause release of endogenous substances that cause insulin resistance.
PK and PD interactions likely not clinically significant but smokers may need ↑
Irinotecan (Camptosar) ↑ Clearance (18%); ↓ serum concentrations of active metabolite SN-38
(∼40%; via induction of glucuronidation); ↓ systemic exposure resulting
in lower hematologic toxicity and may reduce efficacy.
Methadone Possible increase ↑ metabolism (induction of CYP1A2, a minor pathway for
methadone.)- Carefully monitor response upon cessation.
Mexiletine (Mexitil) ↑ Clearance (25%; via oxidation and glucuronidation); ↓ half-life (36%).
Olanzapine (Zyprexa) ↑ Metabolism (induction of CYP1A2): ↑ clearance (98%); ↓ serum
Dosage modifications not routinely recommended but smokers may need
Propranolol (Inderal) ↑ Clearance (77%; via side-chain oxidation and glucuronidation).
Riociguat (Adempas) ↓ Plasma concentrations (by 50%–60%)
Smokers may require dosages higher than 2.5 mg 3 times daily; consider
dose reduction upon cessation.
(30%) and AUC (38%) in study with patients with restless legs
Tacrine (Cognex) Increase ↑ metabolism (induction of CYP1A2); decrease ↓ half-life (50%); serum
concentrations 3-fold lower. -Smokers may need increased ↑ dosages.
Tasimelteon (Hetlioz) Increased ↑ Metabolism (induction of CYP1A2); drug exposure decreased ↓ by
40%. -Smokers may need increased ↑ dosages.
↑ Metabolism (induction of CYP1A2); ↑ clearance (58%–100%); ↓ half-life
Levels should be monitored if smoking is initiated, discontinued, or
↑ Clearance with secondhand smoke exposure.
Maintenance doses are considerably higher in smokers; ↑ Clearance also
with secondhand smoke exposure.
Tizanidine (Zanaflex) ↓ AUC (30%–40%) and ↓ half-life (10%) observed in male smokers.
Possible interaction with tricyclic antidepressants in the direction of ↓ blood levels,
but the clinicalsignificance is not established.
Warfarin ↑ Metabolism (induction of CYP1A2) of R-enantiomer; however, S-enantiomer is
more potent and effect on INR is inconclusive. Consider monitoring INR on
↓ Sedation and drowsiness, possibly caused by nicotine stimulation of central
β-Blockers Less effective antihypertensive and heart rate control effects; possibly caused by
nicotine-mediated sympathetic activation.
Corticosteroids, inhaled Smokers with asthma may have less of a response to inhaled
↑ Risk of cardiovascular adverse effects (e.g., stroke, myocardial
infarction, thromboembolism) in women who smoke and use combined
↑ Risk with age and with heavy smoking (15 or more cigarettes/day) and is
quite marked in women aged 35 and older.
This class of drugs may cause coronary vasospasm; caution for use in smokers
due to possible unrecognized CAD.
Bold rows indicate the most clinically significant interactions.
AUC, area under the curve; Cmax
, maximal concentration; Css, steady state concentration; INR, international
normalized ratio; PD, pharmacodynamics; PK, pharmacokinetics.
The Regents of the University of California. All rights reserved.
Quitting at ages 30, 40, 50, and 60 results in 10, 9, 6, and 3 years of life gained,
1 On average, cigarette smokers die approximately 10 years younger
than do nonsmokers, and of those who continue smoking, at least half will eventually
die as a result of a tobacco-related disease. Persons who quit before age 35 add 10
years of life and have a life expectancy similar to men who had never smoked.
reduction in smoking does not equate to a reduction in harm,
smoking (e.g., 1–4 cigarettes/day) have documented risks.
the number of cigarettes smoked/day should be viewed as a positive step toward
quitting, but should not be recommended as a targeted end point. For any patient who
uses tobacco, the goal is complete, long-term abstinence from all nicotine-containing
Tobacco Use and Dependence: Treatment Approaches
Most tobacco users attempt to quit without assistance, despite the fact that persons
who receive assistance are more likely to be successful in quitting.
complexity of the tobacco dependence syndrome and the constellation of factors that
contribute to tobacco use, treatment requires a multifaceted approach. To assist
clinicians and other specialists in providing cessation treatment to patients who use
tobacco, the US Public Health Service published the Clinical Practice Guideline for
Treating Tobacco Use and Dependence. This document, which represents a
distillation of more than 8,700 published articles,
7 specifies that clinicians can have
an important impact on their patients’ ability to quit. A meta-analysis of 29 studies
estimated that compared with patients who do not receive an intervention from a
clinician, patients who receive a tobacco-cessation intervention from a physician
clinician or a nonphysician clinician are 2.2 and 1.7 times, respectively, more likely
to quit (at 5 or more months after cessation). Although even brief advice from a
clinician has been shown to lead to increased odds of quitting,
counseling yields more dramatic increases in quit rates.
delivery of counseling include group programs
7,31 and telephone counseling.
Numerous effective medications are available for tobacco dependence, and
clinicians should encourage their use by all patients attempting to quit smoking—
except when medically contraindicated or with specific populations for which there
is insufficient evidence of effectiveness (i.e., pregnant women, smokeless tobacco
users, light smokers, adolescents).
7 Although both pharmacotherapy and behavioral
counseling are effective independently, patients’ odds of quitting are substantially
increased when the two approaches are used simultaneously.
significant impact on a patient’s likelihood of success by recommending
pharmacotherapy agents and by supplementing medication use with behavioral
counseling as described later in this chapter.
Assisting Patients with Quitting
BEHAVIORAL COUNSELING STRATEGIES
According to the Clinical Practice Guideline,
five key components constitute
comprehensive counseling for tobacco cessation: (a) asking patients whether they use
tobacco, (b) advising tobacco users to quit, (c) assessing patients’ readiness to quit,
(d) assisting patients with quitting, and (e) arranging follow-up care. These steps are
referred to as the “5 A’s” and are described, in brief, as follows. Figure 91-2 can be
used as a guide for structuring counseling interactions.
Ask: Screening for tobacco use is essential and should be a routine component of
clinical care. The following question can be used to identify tobacco users: “Do
you ever smoke or use any type of tobacco?” At a minimum, tobacco use status
(current, former, never user) and level of use (e.g., number of cigarettes
smoked/day) should be assessed and documented in the medical record. Also,
patients should be asked about exposure to secondhand smoke.
Advise: Tobacco users should be advised to consider quitting; the advice should be
clear and compelling, yet delivered with sensitivity and a tone of voice that
communicates concern and a willingness to assist with quitting. When possible,
messages should be personalized by relating advice to factors such as a patient’s
health status, medication regimen, personal reasons for wanting to quit, or the
impact of tobacco use on others. For example, “I’m concerned because you are on
two different inhalers for your emphysema. Quitting smoking is the single most
important treatment to improve your breathing. I strongly encourage you to quit.
Would you be interested in having me help you with this?”
Assess: Key to the provision of appropriate counseling interventions is the
assessment of a patient’s readiness to quit. Patients should be categorized as
being (a) not ready to quit in the next month; (b) ready to quit in the next month;
(c) a recent quitter, having quit in the past 6 months; or (d) a former user, having
7,35 This classification defines the clinician’s next
step, which is to provide counseling that is tailored to the patient’s level of
readiness to quit. As an example for a current smoker: “Mr. Malkin, what are
your thoughts about quitting, and would you consider quitting sometime in the next
month?” The counseling interventions for patients who are ready to quit will be
different from those for patients who are not considering quitting.
Assist: When counseling tobacco users, it is important that clinicians and patients
view quitting as a process that might take months or even years to achieve. The
goal is to promote forward progress in the process of change, with the target end
point being sustained abstinence from all nicotine-containing products.
When counseling patients who are not ready to quit, an important first step is to
foster motivation. Some patients are not convinced that quitting is important, but most
recognize the need to quit and are simply not ready to make the commitment to do so.
Often, patients have tried to quit multiple times and failed, and thus are too
discouraged to try again. The “5 R’s” can be applied to enhance motivation to quit
(Table 91-2) by clinicians offering to work closely with the patient in designing a
treatment plan. Although it might be useful to educate patients about the
pharmacotherapy options, it is inappropriate to prescribe a treatment regimen for
patients who are not ready to quit. For patients who are not ready to quit in the next
30 days, encourage them to seriously consider quitting and ask the following
Figure 91-2 Tobacco-cessation counseling guide sheet. (Reprinted with permission from Rx for Change:
Enhancing Motivation to Quit: The “5 R’s” for Tobacco-Cessation Counseling
model; effects of secondhand smoke on others, including children and pets).
for socialsupport while quitting, depression, weight gain, and a sense of deprivation or loss.
useful information for the next quit attempt. Repeat interventions when possible.
Rockville, MD: Public Health Service, U.S. Department of Health and Human Services; 2008.
If the patient responds “no,” the clinician should ask, “What would have to change
for you to decide to quit?” If the patient responds “nothing,” then offer to assist, if
or when the patient changes his or her mind. If the patient responds “yes,” the
clinician should continue with question 2.
What might be some benefits of quitting now, instead of later?
The longer a patient smokes, quitting generally becomes more difficult. Most
patients will agree that there is never an ideal time to quit, and procrastinating a
quit date has more negative effects than positive.
What would have to change for you to decide to quit sooner?
This question probes patients’ perceptions of quitting, which reveals some of the
barriers to quitting that can then be discussed.
For patients who are ready to quit (i.e., in the next month), the goal is to work with
the patient in designing an individualized treatment plan, addressing the key issues
listed under the “Assist” component of Figure 91-2.
23 The first steps are to discuss
the patient’s tobacco use history, inquiring about levels of smoking, number of years
smoked, methods used previously for quitting (what worked, what did not work and
why), and reason(s) for previous failed quit attempts. Clinicians should elicit
patients’ opinions about the different medications for quitting and should work with
patients in selecting the quitting methods (e.g., medications, behavioral counseling
programs). Although it is important to recognize that pharmaceutical agents might not
be appropriate, desirable, or affordable for all patients, clinicians should educate
patients that medications, when taken correctly, can substantially increase the
Patients should select a quit date, ideally within the next 2 weeks. This allows
sufficient time to prepare for the quit attempt, including mental preparation,
preparation of the environment, removing all tobacco products and ashtrays from the
home, car, and workspace, and soliciting support their family, friends, and
coworkers. Additional strategies for coping with quitting are shown in Table 91-3.
Patients should be counseled about withdrawal symptoms, medication use, and the
importance of receiving behavioral counseling throughout the quit attempt. Finally,
patients should be commended for taking important steps toward improving their
Arrange: Because patients’ ability to quit increases when multiple counseling
interactions are provided, arranging follow-up counseling is an important element
of treatment for tobacco dependence. Follow-up contact should occur soon after
the quit date, preferably during the first week. A second follow-up contact is
recommended within the first month after quitting.
7 Additional follow-up contacts
should occur to monitor patient progress, assess compliance with
pharmacotherapy regimens, and provide additional support.
Relapse prevention counseling should be part of every follow-up contact with
patients who have recently quit smoking. When counseling recent quitters, it is
important to address challenges in countering withdrawal symptoms and cravings or
temptations to use tobacco. A list of strategies for key triggers or temptations for
tobacco use is provided in Table 91-3.
Importantly, because tobacco use is a
habitual behavior, patients should be advised to alter their daily routines; this helps
disassociate specific behaviors from the use of tobacco. Patients who slip and smoke
a cigarette (or use any form of tobacco) or experience a full relapse back to habitual
tobacco use should be encouraged to think through the scenario in which tobacco use
first occurred and identify the trigger(s) for relapse. This process provides valuable
information for future quit attempts.
All smokers who are trying to quit should be encouraged to use one or more US Food
and Drug Administration (FDA)-approved pharmacologic aids for cessation.
Potential exceptions that require special consideration include medical
contraindications or use in specific populations for which there is insufficient
evidence of effectiveness (i.e., pregnant women, smokeless tobacco users, light
7 Pharmacotherapy should always be combined with
behavioral support and counseling. Currently, the FDA-approved first-line agents
that have been shown to be effective in promoting smoking cessation include five
NRT dosage forms, sustained-release bupropion, and varenicline.
therapy is dictated by considerations such as patient preference for a given agent,
previous experience with cessation medications, current medical conditions,
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