Ramones,Planeta Reina V.

Lung Neoplasms
Lung cancer is the leading cancer killer in the United States. Every year, it accounts for 30% of all cancer deathsmore than cancers of the breast, prostate, and ovary combined. It is the second most frequently diagnosed cancer in the United States, behind prostate cancer in men and breast cancer in women. In the annual report to the nation on the status of cancer in 2007, it was noted that the incidence of lung cancer in men has begun to decrease, while incidence has remained stable in women.

 most patients are diagnosed at an advanced stage of disease, so therapy is rarely curative. The overall 5-year survival for all patients with lung cancer is 15%, which makes lung cancer the most lethal of the leading four cancers.

Epidemiology
Cigarette smoking is the primary cause of lung cancer, with smoking-related cancers accounting for approximately 75% of all lung cancers worldwide in 2007. Two lung cancer types

1. squamous cell carcinoma 2. small cell carcinoma

are extraordinarily rare in the absence of cigarette smoking. The risk of developing lung cancer escalates with the number of cigarettes smoked and the number of years of smoking, and is higher when unfiltered cigarettes are used.

 Even after smoking cessation, however, the risk never drops to that of people who never smoked, regardless of the length of abstinence. Approximately 25% of all lung cancers worldwide and 53% of cancers in women are not related to smoking, and the majority of these (62%) are adenocarcinomas.

 Secondhand (or passive) smoke exposure - has been shown to confer an excess risk of developing lung cancer of 24% when a nonsmoker lives with a smoker.Preexisting lung disease confers an increased risk of lung cancerup to 13%for individuals who have never smoked. This increase is thought to be related to poor clearance of inhaled carcinogens and/or to the effects of chronic inflammation.

 Other causes of lung cancer include : exposure to a number of industrial compounds, including asbestos, arsenic, and chromium compounds. Of particular note is the ominous combination of asbestos exposure and cigarette smoking, which together have a multiplicative effect on risk, as opposed to an additive effect.

 Patients with COPD are at higher risk for lung cancer than would be predicted based on smoking risk alone. A previous history of tuberculosis with secondary scar formation also leads to a higher risk of primary lung carcinoma. Over 3000 chemicals have been identified in tobacco smoke, but the main chemical carcinogens are polycyclic aromatic hydrocarbons. Once inhaled and absorbed, these compounds become mutagenic through their activation by specific enzymes, binding to macromolecules such as DNA and then inducing mutations.

 The lung can be conveniently viewed as two linked components: 1. the tracheobronchial tree (or conducting airways component) 2. the alveolar spaces (or gas exchange component).

 The tracheobronchial tree consists of approximately 23 airway divisions to the level of the alveoli. It includes the: 1. main bronchi 2. lobar bronchi 3. segmental bronchi (to designated bronchopulmonary segments) 4. terminal bronchioles (i.e., the smallest airway vessels, which lack alveoli and are lined by bronchial epithelium).

 The tracheobronchial tree is normally lined by pseudostratified ciliated columnar cells and mucous (or goblet) cells, both of which derive from basal cells. Ciliated cells predominate. Goblet cells which release mucus, can significantly increase in number in acute bronchial injury, such as exposure to cigarette smoke. The normal bronchial epithelium also contains bronchial submucosal glands, which are mixed salivary-type glands containing mucous cells, serous cells, and Kulchitsky cells.

 Kulchitsky cells
- this are neuroendocrine cells -they also are found within the surface epithelium. *The bronchial submucosal glands can give rise to salivary glandtype tumors (previously referred to as bronchial gland tumors), including mucoepidermoid carcinomas and adenoid cystic carcinomas.

 The alveolar spaces or alveoli have two primary cell types, 1. type I pneumocytes -cover 95% of the surface area of the alveolar wall but constitute only 40% of the total number of alveolar epithelial cells. These cells are not capable of regeneration because they have no mitotic potential. 2. type II pneumocytes -cover only 3% of the alveolar surface but constitute 60% of the alveolar epithelial cells. In addition, clusters of neuroendocrine cells are seen in the alveolar spaces.

 Preinvasive Lesions As with epithelial tumors in other organs, precancerous changes can be seen in the respiratory tract. Three precancerous lesions: 1. squamous dysplasia and carcinoma in situ 2. atypical adenomatous hyperplasia 3. diffuse idiopathic pulmonary neuroendocrine cell hyperplasia.

Note:

The term precancerous does not mean that an inevitable progression to invasive carcinoma will occur, but such lesions, particularly those with high-grade dysplasia,do constitute a clear marker of the potential for later development of invasive cancer.

 Squamous Dysplasia and Carcinoma In Situ

Cigarette smoke can induce a metaplastic change of the tracheobronchial pseudostratified epithelium to squamous mucosa, which is a normal response to injury. * With the development of cellular abnormalities in the metaplastic squamous mucosa, squamous dysplasia evolves. * It involves increased cell size, an increased number of cell layers, an increased nucleus:cytoplasm ratio, increased mitoses, and changes in cellular polarity.

 Gradations are considered mild, moderate, or severe.

Carcinoma in situ
- represents carcinoma still confined by the basement membrane.

invasive squamous cell carcinoma

-Once the in situ tumor invades beyond the basement membrane,

 Atypical Adenomatous Hyperplasia

-it is defined as a lesion <5.0 mm consisting of epithelial cells lining the alveoli that are similar to type II pneumocytes.

 Diffuse Idiopathic Pulmonary Neuroendocrine Cell Hyperplasia

- is a rare lesion representing a diffuse proliferation of neuroendocrine cells but without invasion of the basement membrane. - It can exist as a diffuse increase in the number of single neuroendocrine cells or as small lesions <5.0 mm in diameter. - Lesions that are >5.0 mm in size or that breach the basement membrane are carcinoid tumors.