Introduction
 This write up will aim to discuss the pathophysiology, causes and treatment of COPD (Chronic obstructive pulmonary disease), methods of diagnosis pertaining to lung conditions, and the relationship between smoking and lung conditions such as COPD and emphysema. Furthermore, this write up will also discuss the anatomy and physiology of the lungs, mechanisms of breathing as well as lung function recovery post smoking cessation.

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What is COPD?
 Chronic obstructive pulmonary disease (COPD) is a group of lung conditions which cause breathing difficulties. COPD includes 2 conditions: emphysema and chronic bronchitis. Chronic bronchitis is classified by symptoms of excessive sputum production and cough; emphysema refers to chronic shortness of breath, due to enlarged air spaces and damage of lung tissue.1 Risk factors for COPD include smoking. 85% to 90% of COPD cases present in cigarette smokers. Individuals with a history of severe lung infections in childhood are also more likely to develop COPD. The environment which a person lives in may also contribute to the development of COPD, as long-term exposure to air pollution, second-hand smoke and dust, fumes and chemicals (which are often work-related) can cause COPD. Other cases may be the result of a rare inherited genetic problem, such as alpha-1-antitrypsin (a protein involved in lung damage prevention and protection) deficiency. Patients with this deficiency are more vulnerable to alpha-1 deficiency- related emphysema.2 Alpha-1 deficiency related emphysema are usually suspected in patients whom emphysema develops before the age of 40 or those who lack the common risk factors for COPD.1
COPD is a slow progressing disease with an extensive asymptomatic phase, during which lung function declines gradually. Because COPD develops slowly, it is most frequently diagnosed in people aged 40 years or over.3 Common symptoms include increasing dyspnoea, wheezing and chest pain particularly when the patient is active. Other symptoms involve a persistent productive cough with phlegm (this is usually dismissed as a “smokers cough” during the early progression of COPD), and frequent chest infections. Symptoms usually progressively worsen without treatment and may suddenly worsen during flare-ups or exacerbation. Other symptoms of COPD may include weight loss, nutritional abnormalities, and muscle atrophy.1
As the disease progresses, the patient may develop life-threatening complications and exacerbations often. End-stage COPD involves significant dyspnoea even when resting and poses a high risk for lung infections and respiratory failure, and may be life threatening with exacerbation. Patients often succumb to respiratory failure or pulmonary infection. Patients with end-stage COPD usually present with additional clinical symptoms such as low oxygen saturation levels, (thus requiring regular supplements of oxygen), Confusion or dizziness as well as eating difficulty.4
Treatments for COPD may help slow down the progression of the condition, although lung damage due to COPD is usually permanent. The most significant and cost- effective intervention for the progression of COPD in patients is smoking cessation. A number of drugs are effective in promoting smoking cessation, including nicotine replacement products, the antidepressant bupropion (Zyban), the drug varenicline as well as counselling.5 Medications such as bronchodilators used regularly, (alone or in combination) are used for the relieving of symptoms rather than a cure. Especially in mild COPD, long-acting inhaled bronchodilators such as budenoside and salmeterol are more effective and offer greater convenience for patients with mild COPD. These long-acting bronchodilators are usually used in combination with inhaled glucocorticosteroids, which reduce inflammation in the airways and lower mucus production. Short acting bronchodilators such as salbutamol and ipratropium are given to patients during flare-ups or exacerbation for quick relief of symptoms.
End stage COPD patients may also receive additional treatments such as inhaled glucocorticoids, which are prescribed for patients with an FEV1 less than 50 percent of the predicted value and a history of repeated COPD exacerbations. Supplemental oxygen may reduce dyspnoea on exacerbation and improves exercise tolerance in patients with low blood oxygen levels. Non-invasive positive pressure ventilation (NIPPV) may reduce carbon dioxide retention and improve dyspnoea in some patients, however this treatment is not recommended routinely. Pulmonary rehabilitation (a programme of exercise and education for people with chronic lung conditions) has been proven to benefit COPD patients at all stages of the disease. Patients with severe COPD or have not responded to previous treatments (as seen in patients with severe emphysema) may require surgery. Types of surgery include bullectomy (removal of large, abnormal air spaces from lungs) and lung volume reduction surgery.4
How are lung conditions (COPD) diagnosed?
 The standard test used for the diagnosis of lung conditions such as COPD is spirometry. Spirometry is recommended for patients with persistent cough or breathlessness, or if over 35 and smoke. Spirometry can be used to diagnosis conditions such as asthma, COPD, cystic fibrosis and pulmonary fibrosis. It may be conducted to monitor the progression and severity of the condition or response to treatment.6 Spirometry measures 2 key factors: FVC (expiratory forced vital capacity) and FEV1 (Forced expiratory volume in one second). The criterion for diagnosis is based on the FEV1/FVC ratio. The patients’ measurements are compared against normal results of people with the same age, height and sex.
Patients with COPD will have a FEV1/FVC ratio lower than 70%. To decide how mild or severe airflow obstruction is, the criteria below are used.

Figure 1: gradation of severity of airflow obstruction7
According to the Global Initiative for Obstructive Lung Disease (GOLD), there are four stages of COPD. Each stage is classified based on spirometry measurements of FEV1 (the volume of air breathed out in the first second after a forced exhalation).8 The stages of COPD including their gradation based on FEV1/FVC ratios are shown below.

Stage I: Mild COPD. Lung function is starting to decline but may not be noticeable. (FEV1/FVC 80% predicted)
Stage II: Moderate COPD. Symptoms progress, with shortness of breath developing upon exertion. (FEV1/FVC
Stage III: Severe COPD. Shortness of breath worsens and COPD exacerbations are common. (FEV1/FVC
Stage IV: Very severe COPD. Quality of life is gravely impaired. COPD exacerbation may be life-threatening. (FEV1/FVC

In addition, spirometry can be used to determine if the patients’ lung problem is obstructive or restrictive. Patients with obstructive lung conditions (i.e. asthma) can contain normal volumes of air in their lungs, however their ability to exhale is affected by the narrowing of airways. In patients with restrictive lung disease, the amount of air they can inhale is reduced as their lungs are unable to fully expand, as seen in conditions such as pulmonary fibrosis.
The spirometry measurements for obstructive lung diseases are: FEV1 is reduced (0.7). 10 The graphs below depict the spirometry measurements relating to obstructive lung conditions and restrictive lung conditions.

Figure 2: depicting spirometry measurements relating to obstructive lung disease11

Figure 3: depicting spirometry measurements relating to restrictive lung disease11
 In addition to spirometry, other tests for COPD may be done, including a chest X-ray, a blood test to exclude other pathologies, and a full blood count to identify anaemia or polycythaemia. A blood test is also done to identify individuals with alpha-1-antitrypsin deficiency which increases their risk for COPD. Patients may also have their BMI calculated (Being overweight or underweight will determine how well the patient will be able to cope with their COPD)12 A phlegm sample is taken to test for signs of a chest infection, and a peak flow test can be used to exclude an asthma diagnosis.
The relationship between smoking, COPD and lung conditions
 Exposure to cigarette smoke significantly increases the risk of developing emphysema in patients. The inhaled irritants in cigarette smoke cause inflammatory cells to be released from polymorphonuclear leukocytes and alveolar macrophages to move into the lungs. Inflammatory cells are known as proteolytic enzymes (such as serine elastase), which the lungs are usually protected from due to the actions of alpha1-antitrypsin. However, the contents in smoke, such as free radicals (superoxide) destroy alpha-1-antitrypsin, reducing its activity. Therefore, emphysema develops when the production and activity of this antiprotease are not enough to counter the harmful effects of excess serine elastase production.  Serine elastase then destroys the elastic tissues and collagen in the alveolar walls of the lung, leading to a reduction in the lung surface area for gas exchange.13

Figure 4: depiction of how cigarette smoke and alpha-1-antitrypsin deficiency results in alveolar tissue damage and the development of emphysema13
 The inhalation of cigarette smoke adversely affects lung function through a series of changes in normal function of lung tissue. As chemicals from cigarette smoke enter the lungs, the lining of lungs become inflamed, after several hours cilia lining the lungs become temporarily paralysed and less efficient at removing mucus and other substances (i.e. dust and pathogens) from the airways. Additional changes to the lungs of smokers include an increase in the thickness and production of mucus. Due to the impaired function of cilia, mucus accumulates in the airways, resulting in productive cough and increased risk of lung infections.14 Long term exposure to damaging chemicals in cigarette smoke lead to scarring and inflammation of lung tissue, loss in elasticity of lungs and decreased gas exchange efficiency.
Anatomy and physiology of the lungs, and the basic mechanisms of breathing
Each lung is covered in a serous pleural sac consisting of two continuous membranes, the parietal and visceral pleura. The parietal pleura line the pulmonary cavity and adhere to the thoracic wall, mediastinum and diaphragm. The potential space between the visceral and parietal layers contains a layer of serous pleural fluid which lubricates the pleural surfaces and allows the layers to slide smoothly over each other during respiration. Surface tension created by the pleural cavity provides the cohesion that keeps the lung surface in contact with the thoracic wall.15
 The airways of the lungs divide 23 times in total: The first 16 divisions constitute the conducting airways (which end with terminal bronchioles). The last 7 divisions constitute the respiratory zone (starting from respiratory bronchioles). There are about 8 million alveolar ducts in each lung, which each divide into terminal alveolar sacs. Gas exchange takes place in the alveoli. Alveoli contain surfactant to prevent their collapse during inhalation. Pulmonary Surfactant is made up of a complex mixture of lipid and proteins secreted by the type II pneumocytes and lowers tension within the alveoli.
Anatomically, the right lung is made up of 3 lobes (superior lobe, middle lobe and inferior lobe). The superior lobe is separated from the middle lobe by the horizontal fissure; the middle lobe is separated from the inferior lobe by the oblique fissure). The left lung is made up of 2 lobes, the superior lobe and inferior lobe, which are separated by the oblique fissure. A cardiac notch is present medially to the superior lobe.

Figure 5: lobes and fissures of the lungs14
Inspiration and expiration are dependent on the differences in pressure between the atmosphere and the lungs. Boyles law refers to the relationship between volume and pressure in a gas at a constant temperature, and states that the pressure of a gas is inversely proportional to its volume.16 Gas flows from regions of high pressure to regions of low pressure. These principles apply to mechanisms of breathing during inhalation and exhalation.
During inhalation, the external intercostals muscles contract, moving the rib cage up and out, and the diaphragm contracts and lowers. The volume of the thoracic cavity increases, thus pressure in the lungs decreases, and air is drawn into the lungs. Air fills the lungs because the pressure within the thoracic cavity is less than the atmospheric pressure. Air continues to flow until the pressure inside the lungs rises to the atmospheric pressure. The muscles involved during forced or deep inhalation are the sternocleidomastoid muscle, scalene muscles and pectoralis minor.
During exhalation, most of the air in the thoracic cavity moves out of the lungs by elastic recoil of structures within the thoracic cavity. During deep or forced exhalation, the abdominal muscles and internal intercostals muscles contract moving the rib cage down and in, the diaphragm relaxes, pushing the diaphragm up, and the volume of the thoracic cavity decreases, thus air is forced out of the lungs. Air exits the lungs because the pressure within the thoracic cavity is greater than the atmospheric pressure. Air continues to flow until the pressure inside the lungs drops to the atmospheric pressure.

Figure 6: inhalation and exhalation16
Lung recovery after smoking cessation
After quitting smoking, some of the short-term inflammatory changes to the lungs can be reversed. However, smoking- induced emphysema involves the destruction of alveoli in the lungs, which is irreversible. Swelling subsides on the surface of the lungs and airways, and lung cells produce less mucus. New cilia can grow, which are more efficient at removing mucus and clearing other substances from the lungs. In addition, inflammation of the linings of airways decreases when the lining is no longer exposed to the chemical irritants found in cigarette smoke. Lung damage and deterioration in lung function are directly related to the number of pack years. The likelihood of irreversible damage to the lungs also increases linearly with the amount of pack years.14
Conclusion
 In conclusion, this write up explored Annie Kennedy’s COPD prognosis, the physiological processes involved in emphysema and COPD conditions, as well as physiological processes of normal lung function and changes in these processes as a result of smoking.
REFERENCE SECTION
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