Lung cancer (teratment)

- The treatment of lung cancer is dependent on the type and stage of cancer.
- The treatment explained here is only a summary:

1) Non-small cell lung cancer

* Stages IA, IB, IIA, IIB & some IIIA :

- basically the tumour is resected with / without removal of the lymph nodes in the mediastinum.
- post-operative radiotherapy is only advocated for selective patients.(with N2 disease if no neoadjuvant chemotherapy)

* Stage IIIA & IIIB

- The treatment for this stage of lung cancer is a little more complicated in that it depends also on the nature of the tumour i.e. bulky, with/without chest wall invasion,etc.
- It is suffice to say that resection of tumour is followed up with chemotherapy or radiotherapy.

* Stage IV & more advanced IIIB

- For this stage, radiotherapy to site of the involved area for relieve of symptoms.
- Chemotherapy for ambulatory patients.
- Resection of primary tumour and tumour spread (metastases) will be considered.

2) Small cell lung cancer

- limited stage (good performance status) : chemotherapy + chest radiotherapy
- Extensive stage (good performance status) : combination chemotherapy
- complete tumour responders (all stages) : consider prophylactic cranial radiotherapy
- Poor-performanc-status patients (all stages) :modified-dose combination, palliative care.

3) All patients

- radiotherapy for brain metastases, spinal cord compression, weight bearing lytic bony lesions, symptomatic local lesions.
- encourage to stop smoking.
- supportive care during chemotherapy.

Lung cancer (Histological classification)

Bronchogenic carcinomas of primary lung cancers can be classified as follows:

o Non small cell lung carcinomas (NSCLC) : This accounts for 70 -75% of bronchogenic carcinomas and can be further subdivided into:

§ Squamous cell carcinoma (25-30%)

§ Adenocarcinoma (30-35%)

§ Large cell carcinoma (10-15%)

o Small cell lung carcinoma (SCLC) : This chalks up 20 – 25% of bronchogenic carcinomas and comprises mainly of a group of cancers called oat cell carcinomas.

o Combined patterns : this consists of the various types of combinations of NSCLC and SCLC e.g. combined squamous & adenocarcinomas and combined squamous cell carcinomas & SCLC.

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

Lung Cancer

- Lung cancers or lung neoplasms can be generally divided into 3 broad categories, namely:

• Primary lung cancer (where cancer develops in the lung tissue itself)
• Secondary lung cancer (due to deposits of cancer cells originating from other cancer organs)
• Mesothelioma (cancer of the layer of tissue (pleura) that surrounds the lung ) - not really a lung cancer per se.

- Primary lung cancers can be further classified into

• benign (cancers that do not spread to other organs)
• malignant (cancers that do spread)

- More than 20 bengin & malignant primary lung cancers have been identified & classified histologically.

- However, 90 - 95% of these lung cancers are bronchogenic carcinomas.

- About 5% are bronchial carcinoids and 2 - 5% are mesenchymal & other miscellaneous lung cancers.

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 (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).