Lung cancer (Incidents and risk factors)

- Lung cancer accounts for around 19% of all cancers and 27% of cancer deaths.

- The incidence is increasing in women (due to the increase in women smokers).

- The major risk factor for lung cancer is cigarette smoking.

- Other risk factors:

o Passive smoking - being near smokers and inhaling the smoke which is being exhaled by smokers increases the risk to twice that of non-smokers.

o Heavy metal exposure - exposure / working with heavy metals e.g. nickel, chromium, vinyl chloride, arsenic for prolonged periods of time.

o Asbestos exposure - increases the risk of non-smokers by 5 fold & 55 times greater in smokers.

o Chronic Obstructive Pulmonary Disease (COPD) (check out my writings on COPD)

o Industrial carcinogens - products from factories that cause cancer e.g. chloromethyl ether.

o Lung scars - e.g. post-tuberculosis infection

o Air pollution - prolonged exposure

o Hereditary - genetic factors

COPD (treatment)

Smoking cessation

· Since smoking is the main cause for COPD, stopping is definitely the treatment option. This has proved to prolong the survival in patients with COPD.

· Although lost lung function is not regained, the lung damage stops. (rate of FEV₁ reverts back to that of non-smokers)

· For those who can’t stop smoking without an aid, replacement therapy such as nicotine patch, gum or inhaler helps to some certain extend. (user dependant)

· Oral medication to help smoking cessation is another alternative. (e.g. bupropion)

Bronchodilators

· These are medications used to enlarge a narrow airway by action of relaxing the muscles around the airway.

· There are short acting (medication that last only a short period of time after use) & long acting bronchodilators.

· The bronchodilators are in inhaler or oral preparations. (However, inhaled medications have fewer side effects)

· Examples are ipratropium (short acting) and salmeterol (long acting). Theophylline’s use is limited due to its’ narrow therapeutic range. (this means that the individual taking this medication is at a higher risk of getting toxic levels of the medication thus increasing the adverse effects)

Oxygen

· This therapy can be given at home (if the equipment and operator skills are available).

· The therapy shows reduced symptoms & improved survival in patients with COPD. (provided they have stopped smoking)

· The oxygen saturation (Sa_O2) is best kept above 90%.

Lung transplant

· This is only done if all methods of treatment above are tried and have failed & the function of the lung is severely low.(FEV₁ is less than 25%)

Lung volume reduction surgery

· Still another method used to help patients with COPD.

· However, this is a highly specific treatment for a selected group of COPD patients.

COPD (signs & symptoms)

Do you have COPD?

Symptoms of COPD

- symptom is the change in the body's structure, function, or sensation, experienced by the patient & indicative of disease.

1. cough with phlegm
2. breathlessness on mid exertion
3. wheeze (breathing with difficulty & noisily)

Signs of COPD

- sign is an objective indication of disease, discoverable on examination of the patient (usually) by a physician.

- early signs

1. wheezing upon exhalation

- late signs

1. tachypnoea (rapid breathing-the definition varies with the age of the patient)
2. hyperinflated chest (over expansion / distension of chest)
3. marked widespread wheeze
4. 'Pink puffers' or 'blue bloaters'

COPD & smoking

Why does smoking causes COPD?

- In a smoker's lung, there are basically two things that take place:

1. the lung reacts to smoke particles (e.g. nicotine, tar) => know as indirect injury
2. the smoke particles react to the lung => known as direct injury

- Indirect injury:

• In smokers, there is an accumulation of immune cells (immune cells protecting the body are liken to the policemen & soldiers that protect a country) within the alveoli. (remember the tree analogy? These are the leaves)
• It is believed that the immune cells (neutrophils and macrophages) are attracted to the lung alveoli by the smoke particles, nicotine. (as an action of local immune cells.)
• Of the 2 immune cells, 1 of them (neutrophils) release a variety of protein substances (e.g.neutrophil elastase, proteinase 3 & cathepsin G) finally resulting in lung alveolar damage.
• The other immune cell (macrophage) also releases a protein substance calledmetalloproteinase which causes additional damage to the lung alveoli. (It's just like a war occuring within a country's gates. When bullets are fired, innocent people get hurt too.)

- Direct injury:

• Smoking plays a role in causing direct injury to the lungs by producing harmful products known as reactive oxygen species / "free radicals".
• Free radicals cause lung alveolar damage by destroying the 'guys' that maintain the well-being of the alveoli (known as alpha 1 anti-trypsin)

- All these insults results in the loss of alveolar attachments (supporting structure) & thus acollapse of brochial wall upon breathing. (this is what happens in emphysema)

- The continuous insult in the alveoli causes deposits of hardening tissue (fibrosis) hence thenarrowing of airflow and airway limitation. (this is chronic bronchitis)

COPD (causes)

Causes of COPD/COAD

- Chronic Obstructive Pulmonary Disease (COPD) commonly occurs in individualsover the age of 35. (It is a progressive disease, therefore it takes time to show physical signs.)

- The single and most inportant cause of COPD is smoking. (Why? check out the next update!!)

- Did you know that in 90% of patients suffering from COPD, it is the result of long-term heavy cigarette smoking? The remaining 10% are non-smokers who develop COPD for which the reason is still uncertain. (medical X-files ^_^)

- In the majority of clinical settings, a patient either has COPD or asthma, not both. However, although asthma (reversible, over-reactive airway) is a distinct disorder, it may be a part of COPD in some patients. (but this is for the respiratory specialist to crack their heads over. ^_^)

- For the past few decades, the increase in smoking, environmental pollutants, and other noxious gas exposures has caused the incidence of COPD to rise dramatically.

-COPD is even ranked in the top 5 causes of morbidity(a diseased state) worldwide.

- Other causes of COPD would include occupational dust exposure (e.g. coal miners) & repeated lung infections. (e.g. tuberculosis)

COPD (Introduction)

COPD (Chronic Obstructive Pulmonary Disease) / COAD (Chronic Obstructive Airway Disease)

Introduction:

COPD and COAD are the one and the same. The usage of the terms depends on the country you come from. (^_^)

Definition:

- Lung disease are generally grouped into 2 categories, namely obstructive & restrictive diseases.

- Obstructive disease

• means - an increase resistance to air flow
• due to partial / complete obstruction
• at any level of the airway

- Restrictive disease

• means - a decrease in the ability of the lung to expand
• and - a decrease in the lung's air storage capacity

-COPD falls under the obstructive category of lung diseases. (However, note that there are no absolutes in the medical line. There are COPDs without obstructive elements! )

[NB: a tip for medical or nursing students in answering exam questions - if there is an answer to a question which states words such as ALL or NEVER or anything along that line, the chances that the answer is wrong is certain.(^_^)]

-COPD is a common progressive obstructive disorder ofthe airway with little or no reversibility.

-Clinically, COPD includes a combination of

• chronic bronchitis (a person with persistent productive cough for most days, in at least 2 consecutive years)
• emphysema (a person with permanent increase of air spaces beyond the normal size, at the level away from the terminal bronchioles-in other words, alveolar region)
• Think of the lung as an inverted tree, with it's trunk (trechea) slowly progressing to the leaves. The twigs of the tree are the bronchioles and the leaves are the alveoli / terminal sac.
• accompanied by destruction of their walls
• with / without obvious deposits of hardening tissue (due to reactive process to the disease).