The Respiratory System

at a Glance

Jeremy Ward, Jane Ward and Richard Leach

Case Studies

Case 7

The wife and daughter of a patient you are treating for lung cancer are concerned about their risk of developing cancer. The wife has smoked for 40 years and has a 40-pack/year history but is keen to stop. The daughter has never smoked but has had lifelong passive cigarette-smoke exposure.

  • 1. What are the risks associated with cigarette smoking?

    Correct answer:
    Smoking accounts for 90% of lung cancer cases and approximately 30% of all cancer deaths in developed countries. Cancers of the oropharynx, nasal cavity, nasal sinuses, larynx, oesophagus, stomach, pancreas, liver, urinary tract, uterine cervix and myeloid leukaemia are all associated with smoking. In the United Kingdom in 2005, 46,000 cancer deaths were attributed to smoking. Smoking also causes chronic obstructive pulmonary disease (COPD), coronary heart disease, peripheral vascular disease, stroke, pneumonia, interstitial lung disease, venous thromboembolism, diabetes, inflammatory bowel disease and peptic ulceration. The relative risk of developing lung cancer in a long-term smoker compared to a lifelong non-smoker is increased by about 30-fold. The level of risk is dependent on dose (i.e. number of cigarettes/day, depth of inhalation and number of years smoked), age of onset, race (e.g. African-Americans at greater risk) and pattern of smoking (i.e. a quit period reduces subsequent risk on restarting smoking).

  • 2. Why is smoking addictive?

    Correct answer:
    High brain nicotine levels occur within 7–10 seconds of inhaling cigarette smoke. Activation of brain nicotine acetylcholine receptors (nAchR) stimulates the release of neurotransmitters (e.g. noradrenaline and serotonin), especially dopamine in the mesolimbic system (brain reward pathway), which elicits pleasure and is associated with the development of addictive behaviour. Repeated exposure to nicotine desensitises nAchR, and despite a 300% increase in the number of receptors, the response to nicotine gradually decreases and natural brain dopamine levels fall, requiring increased nicotine stimulation for equivalent effect.

  • 3. How would you advise the wife regarding smoking cessation?

    Correct answer:
    Smoking cessation is best achieved using a combination of intensive behavioural support and pharmacological therapies. Initially assess the 5As:
    Ask how much the person smokes and document pack years
    Assess risk of continued smoking and inform the patient
    Advise how to stop smoking and what help is available
    Assist with behavioural support or replacement therapy and
    Arrange follow-up.
    It is vital that the patient is well motivated and has set a quit date to stop smoking completely (i.e. ‘to go cold turkey’). Slowly reducing daily cigarette consumption will not overcome the additive nature of smoking. Quit rates with simple counselling are only 1–3%, but intensive behavioural support with telephone follow-up, web-based support and multiple interviews can achieve 20% one-year abstinence rates. Nicotine replacement therapy (NRT) is the most used pharmacological aid to smoking cessation. A 22 mg patch raises the baseline blood nicotine concentration to levels achieved by smoking 30 cigarettes over 24 hours. However, addition of gum or lozenges to the patch helps overcome breakthrough urges. When intensive smoking cessation support is combined with NRT, 1–year abstinence rates of 35% can be achieved. Bupropion (Zyban), a dopamine uptake inhibitor, doubles the success of smoking cessation. It is started 1–2 weeks before stopping smoking and is given for 8 weeks. Combination with NRT is not always beneficial. Bupropion is contraindicated in epilepsy and pregnancy. Varenicline (Champix) is a new partial nAchR agonist that reduces craving and withdrawal and decreases the reward of smoking. A 12-week course is recommended and is commenced 1–2 weeks before the ‘quit date’. Twelve-week quit rates in two major studies comparing vareniciline, bupropion and placebo were 45, 30 and 18%, respectively, and at 12 months were 23, 16 and 9%, respectively.

  • 4. Following smoking cessation what is the risk of developing cancer?

    Correct answer:
    Smoking cessation reduces the risk of developing lung cancer by up to 90%. However, the risk of developing lung cancer is always higher than in lifelong non-smokers and is dependent on the number of cigarettes smoked, age at smoking cessation and the number of years since smoking cessation. For every year smoking cessation is postponed after 40 years old, life expectancy is reduced by 3 months. Passive smoking is associated with both morbidity and mortality. Non-smokers who live with smokers have a 24% increase in the incidence of lung cancer. The risk is 16–19% in those exposed to passive smoking in the workplace.

  • 5. What are the effects of passive smoking on children?

    Correct answer:
    Passive smoking is harmful in children and increases respiratory disease, asthma attacks, cot deaths and middle ear infections. In the United Kingdom over 30% of children live with at least one adult smoker, and among low-income families this increases to 57%. Smoking during pregnancy is associated with increased risk of spontaneous abortion, preterm birth, low birth weight and stillbirth. In 2005, 32% of women smoked before or during pregnancy and 17% throughout pregnancy. These figures were 48 and 29%, respectively, in lower socioeconomc groups.

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