Bronchogenic Carcinoma is a primary malignant tumor originating from lung airways.
In the literature always reported an increased incidence of lung cancer in a progressive, not only as a result of increased average age of humans and better diagnostic capability, but because it is more common carcinoma bronchogenic
Such as cancer in general, the exact etiology of carcinoma bronchogenic still unknown, but it is expected that the long-term inhalation of carcinogenic materials is a major factor, without prejudice to possible predisposing role of family relations or ethnic / racial and immunologis status. Inhalation of carcinogenic materials is highlighted that many cigarettes.
Effect of cigarette:
The materials are carcinogens in tobacco smoke include: polomium 210 and 3.4 benzypyrene. The use of a filter is said to reduce the risk of bronchogenic carcinoma , but still remained higher than non-smokers.

In the long term ie, 10-20 years, smoking:
1-10 cigarettes / day increases the risk 15 times
20-30 cigarettes / day increases the risk 40-50 times
40-50 cigarettes / day increases the risk 70-80 times.

Industry Influence
The most widely associated with the carcinogen is asbestos, which otherwise increases the risk of cancer is 60-10 times. Following the industrial radioactive materials, miners uramium 4 times the population at risk in general. Exposure to this industry only visible effect after the 15-20 years.

Effect of Other Diseases
Tuberculosis been associated as lung carcinoma brinkogenik predisposing factors, through mechanisms hyperplasi - metaplasi - carcinoma in situ-carcinoma - bronkogenik as a result of scar tissue tuberculosis.

Effect of Genetic and immunological status
In 1954, Tokuhotu can prove that despite the influence of heredity rather than factors of environmental exposure, this provides an opinion that can be derived bronkogenik carcinoma. Research recently skewed that the factors involved with Aryl Hydrocarbon hydroxylase enzymes (AHH). Status immonologis patients are monitored from cellular mediated showed a correlation between the degree of cell differentiation, stage of disease, response to treatment and prognosis. Patients are generally not the energy to respond more quickly to treatment and died.

Classification by histopathology using ordinary light microscope (WHO, 1977).
1. Epidermois carcinoma (squamous cell carcinoma).
2. Adeno carcinoma
3. Undiferentiated small cell carcinoma (oat cell)
4. Large cell carcinoma undeferentiated.

Primary lung cancer usually histologinya classified by type, all have a natural history and response to the berbeda0beda pengibatan. Although there are more than a dozen types of primary lung cancer, but cancer bronkogenik, including the first four types of cells, represents 95% of all lung cancers.
Based on treatment options, the carcinoma bronchogenic usually divided into Small Cell Lung Cancer(SCLC) and Neoplasma Small Cell Lung Cancer (NSCLC).

Supporting Data
1. Radiological
a. Radiopaque mass in the lung
b. Airway obstruction with resultant atelectasis
c. Pneumonia
d. Enlarged hilar glands
e. Cavitation
f. Tumor Pancoast.Ca. Bronchogenic contained disuperior pulmonary sulcus, the superior lobe stale.
g. Abnormalities in the pleural
h. Bone disorders

2. Bronkografi
The picture is considered bronkografi patognomonik irregular stenosis is obstruction, stenosis rats and indented thumb.

3. Cytology
Representative sputum can be obtained through spontaneous cough, with the help of aerosols (20% propylene glycol in 10% NaCl solution. Warmed to approximately 45-50 C.) or through rinsing / sweep aspiration bronkial.Tatalaksana on Lung Cancer Detection Program at New York is as follows. Saliva and nasal discharge post removed first, then the patient asked to cough deeply, resulting sputum were fixed immediately, all of which are performed on 3 consecutive days, preferably in the morning.

4. Endoscopy
Includes examining laryngoscopy and bronchoscopy and bronchial washings, scrapings / sweep and biopsy. The objective examination of bronchoscopy (fiber optics) are:

a. Knowing the changes in the bronchus of lung cancer.
b. Retrieving material for cytological examination.
c. Noting the changes on the surface of tumor / mucosa to estimate the type of malignancy.
d. Assessing the success of therapy.
e. Determining operbilitas lung cancer.

5. Biopsy
Biopsy material can be obtained by means of percutaneous biopsy or open biopsy transbronkial. While the material can form a network of regional lymph tissue pleural or lung tissue.

6. Immunology
The existence of a negative correlation between cancer and imunologic reaction has been generally known. Impaired imunulogik especially visible in Cell mediated immunity that can be given through a bored delayed hypersensitivity reaction, tolerance to skin graft, the number of circulatory renadh T cells, and lymphocyte transformation in vitro is low. At this time more imunulogik examination acts as a prognostic factor rather than a diagnostic factor. Conclusion Correlation of skin test and response to sitostatica:
a. Less than 1.0 cm. : Prognosis is poor, widespread disease.
b. Less than 2.5 m. ; Better prognosis, limited disease, good response to chemotherapy

Clinical Staging
Based on TNM.
T = Tumor: N. : Nodules, namely the lymph nodes of M. : Metastases
T-0: No visible primary tumor
T-1: tumor diameter of less than 3 cm. Without the invasion of bronchus
T-2: tumor diameter more than 3 cm. Can be accompanied by atelectasis or pneumonitis, but is more than 2 cm. From Karina, and yet adaefusi pleura.
T-3: Tumor size with an invasion into the surrounding (thoracic wall, diaphragm or mediatinum) or have been near carina accompanied by pleural effusion.
N-0: There was no propagation to regional lymph nodes.
N-1: There is a propagation to the ipsilateral hilar lymph nodes.
N-2: There is a spreading to the lymph limfemediastinum or contralateral
N-3: There ekstratorakal spreading to lymph nodes.
M. M-0: There is no distant metastases.
M-1: Already there are metastae far into other organs.
Based on TNM. Compiled phasing following clinics.
a. Carcinoma in situ: T-0, N-0, M-0, but positive sputum cytology for malignant cells.
c. Phase I. T-1, N-0, M-0, or T-2, N-0, M-0
d. Phase II. T-2, N-1,, M-0.
e. Stage III: when there are already T-3, N-2, or M-1.

Tag : Cancer bronchogenic, Lung Cancer, cancer lung airways, Small Cell Lung Cancer(SCLC), Neoplasma Small Cell Lung Cancer (NSCLC)