انت هنا الان : شبكة جامعة بابل > موقع الكلية > نظام التعليم الالكتروني > مشاهدة المحاضرة
الكلية كلية طب الاسنان
القسم العلوم الاساسية
المرحلة 3
أستاذ المادة علي زكي ناجي الاسدي
5/31/2011 7:54:43 AM
PNEUMOCONIOSES
The term pneumoconiosis describe the non-neoplastic lung reaction to inhalation of mineral dusts (e.g., coal dust anthracosis, silica silicosis, asbestos asbestosis, and beryllium berylliosis) commonly encountered in the workplace. Although the pneumoconioses result from well-defined occupational exposure to specific airborne agents, there are also important effects of particulate air pollution for the general population, especially in urban areas.
General Pathogenesis. The amount of dust retained in the lungs is determined by the dust concentration in the air, the duration of the exposure, and the effectiveness of clearance mechanisms.
(1) any influence, such as cigarette smoking, that affects the integrity of the mucociliary apparatus significantly predisposes to the accumulation of dust, and
(2) the most dangerous particles range from 1 to 5 mm in diameter because they may reach the terminal small airways and air sacs and settle in their linings. Under normal conditions, there is always a small pool of intra-alveolar macrophages that is expanded by recruitment of more macrophages when dust reaches the alveolar spaces. The protection provided by phagocytosis of particles, however, can be overwhelmed by the large dust burden deposited in occupational exposures. These tend to evoke fibrosing collagenous pneumoconioses, silica tend to trigger macrophages to release a number of products that mediate an inflammatory response and initiate fibroblast proliferation and collagen deposition. Some of the particles may be taken up by epithelial cells or may cross the epithelial cell lining and interact directly with fibroblasts and interstitial macrophages. Some may reach the lymphatics either by direct drainage or within migrating macrophages and thereby initiate an immune response to components of the particulates or to self-proteins (or both), modified by the particles. This response leads to an amplification and extension of the local reaction. Although tobacco smoking worsens the effects of all inhaled mineral dusts, the effects of asbestos are particularly magnified by smoking.
Coal Workers Pneumoconiosis: Coal, a form of combustible carbon, has long been mined for fuel. The spectrum of lung findings in coal workers is wide, varying from
1) asymptomatic anthracosis, in which pigment accumulates without a perceptible cellular reaction.
2) simple coal workers pneumoconiosis (CWP), in which accumulations of macrophages occur with little to no pulmonary dysfunction.
3) complicated CWP, or progressive massive fibrosis (PMF), in which fibrosis is extensive and lung function is compromised. Morphology: Anthracosis is the most innocuous coal-induced pulmonary lesion in coal miners and is also commonly seen in all urban dwellers and tobacco smokers. Inhaled carbon pigment is engulfed by alveolar or interstitial macrophages, which then accumulate in the connective tissue along the lymphatics, including the pleural lymphatics, or in organized lymphoid tissue along the bronchi or in the lung hilus. At autopsy, linear streaks and aggregates of anthracotic pigment readily identify pulmonary lymphatics and mark the pulmonary lymph nodes. Simple CWP is characterized by coal macules (1 to 2 mm in diameter) and the somewhat larger coal nodules. The coal macule consists of carbon-laden macrophages; the nodule also contains small amounts of a delicate network of collagen fibers. Although these lesions are scattered throughout the lung, the upper lobes and upper zones of the lower lobes are more heavily involved. They are located primarily adjacent to respiratory bronchioles, the site of initial dust accumulation. In due course, dilation of adjacent alveoli occurs, a condition sometimes referred to as centrilobular emphysema. By definition, emphysema is associated with destruction of alveolar septa, and whether this occurs in primary CWP is not yet certain. Complicated CWP (PMF) occurs on a background of simple CWP and generally requires many years to develop. It is characterized by intensely blackened scars larger than 2 cm, sometimes up to 10 cm in greatest diameter. They are usually multiple.
Microscopically the lesions consist of dense collagen and pigment. The center of the lesion is often necrotic, resulting most likely from local ischemia.
Clinical Course. CWP is usually a benign disease that causes little decrement in lung function.. In a minority of cases, however, PMF develops, leading to increasing pulmonary dysfunction, pulmonary hypertension, and cor pulmonale. Once PMF develops, it may become progressive even if further exposure to dust is prevented. The incidence of clinical tuberculosis is increased in persons with CWP, but whether this reflects a greater vulnerability to infection or, instead, socioeconomic factors inherent in the life of miners is unclear. There is also some evidence that exposure to coal dust increases the incidence of chronic bronchitis and emphysema, independent of smoking, thus complicating the management of the patient with CWP. To date, however, there is no compelling evidence that CWP in the absence of smoking predisposes to cancer.
PULMONARY TUBERCULOSIS Pulmonary involvement is still the major cause of tuberculosis morbidity and mortality. The prevention and control of these pulmonary infections account for tuberculosis being a relatively uncommon cause of death today in the United States. The incidence of this infection in the United States began to increase again in the past decade, however, primarily reflecting infections in patients with acquired immunodeficiency syndrome (AIDS). Moreover, in many parts of the world, underprivileged populations still suffer from death rates 20 times those of industrialized nations, and high-incidence pockets of infection are found among the poor in the most affluent countries.
Primary Pulmonary Tuberculosis: Except for the rare intestinal (bovine) tuberculosis and the even more uncommon skin, oropharyngeal, and lymphoidal primary sites, the lungs are the usual location of primary infections, the initial focus of primary infection is the Ghon complex, which consists of
(1) a parenchymal subpleural lesion, often just above or just below the interlobar fissure between the upper and the lower lobes, and
(2) enlarged caseous lymph nodes draining the parenchymal focus The course and fate of this initial infection are variable, but in most cases patients are asymptomatic, and the lesions undergo fibrosis and calcification. Exceptionally, particularly in infants and children or immunodeficient adults, progressive spread with cavitation, tuberculous pneumonia, or miliary tuberculosis may follow a primary infection.
Secondary (Reactivation) Pulmonary Tuberculosis: Most cases of secondary pulmonary tuberculosis represent reactivation of an old, possibly sub-clinical infection. During primary infection, bacilli may disseminate, without producing symptoms, and establish themselves in sites with high oxygen tension, particularly the lung apices. Reactivation in such sites occurs in no more than 5 to 10% of the cases of primary infection. Secondary tuberculosis, however, tends to produce more damage to the lungs than does primary tuberculosis.
Morphology. The secondary pulmonary tuberculous lesion is located in the apex of one or both lungs. It begins as a small focus of consolidation, usually less than 3 cm in diameter. In almost every case of reinfection, the regional nodes develop foci of similar tuberculous activity. In the favorable case, the initial parenchymal focus develops a small area of caseation necrosis that does not cavitate because it fails to communicate with a bronchus or bronchiole. The usual course is one of progressive fibrous encapsulation, leaving only fibrocalcific scars that depress and pucker the pleural surface and cause focal pleural adhesions. Sometimes, these fibrocalcific scars become secondarily blackened by anthracotic pigment.
Histologically, coalescent granulomas are present, composed of epithelioid cells surrounded by a zone of fibroblasts and lymphocytes that usually contains Langhans giant cells. Some necrosis (caseation) is usually present in the centers of these tubercles, the amount being entirely dependent on the sensitization of the patient and the virulence of the organisms. As the lesions progress, more tubercles coalesce to create a confluent area of consolidation. In the favorable case, either the entire area is eventually converted to a fibrocalcific scar, or the residual caseous debris becomes totally and heavily walled off by hyaline collagenous connective tissue. In these late lesions, the multinucleate giant cells tend to disappear. In cases of suspected tuberculous tissue changes, the diagnosis is confirmed by histologic staining, smears, and cultures of acid-fast organisms.
MILIARY TUBERCULOSIS. Lympho-hematogenous dissemination may give rise to miliary tuberculosis, may confined to the lungs or involving other organs also. The distribution of miliary lesions depends on the pathways of dissemination. Tuberculous infection may drain via the lymphatics through the major lymphatic ducts into the right side of the heart, then spread into a diffuse, blood-borne pattern throughout the lungs alone. Despite their small size, most of the bacilli are usually filtered out by the alveolar capillary bed. Therefore, the infective material may not reach the arterial systemic circulation. Such limitation to the lungs usually is not complete, however, and some bacilli pass through the capillaries or through lymphatic-vascular anastomoses to enter the systemic circulation and produce distant organ seedings. In the miliary type of distribution, individual lesions vary from one to several millimeters in diameter and are distinct, yellow-white, firm areas of consolidation that usually do not have grossly visible central caseation necrosis or cavitation at the time of examination Histologically, however, these present the characteristic pattern of individual or multiple confluent tubercles having microscopic central caseation.
Bronchogenic carcinoma: It is the second most common malignancy in men; it alone accounts for approximately one third of all cancer deaths in men. The incidence is increasing dramatically in women, and lung cancer has passed breast carcinoma as a cause of cancer death in women. Overall, lung cancer is the most frequent fatal malignancy. Cancer of the lung occurs most often between ages 40 and 70 years, with a peak incidence in the fifties or sixties. Only 2% of all cases appear before the age of 40.
Etiology and Pathogenesis
1-Tobacco Smoking. positive relationship between tobacco smoking and lung cancer. the amount of daily smoking, the duration of the smoking habit. Compared with nonsmokers, average smokers of cigarettes have a 10-fold greater risk of developing lung cancer, and heavy smokers (more than 40 cigarettes per day for several years) have at least a 20-fold greater risk. Cessation of smoking for 10 years reduces risk to control levels. Epidemiologic studies also show an association between cigarette smoking and the following cancers: lip, tongue, floor of the mouth, pharynx, larynx, esophagus, urinary bladder, pancreas, and kidney. Cigar and pipe smoking increase risk, although much more modestly than smoking of cigarettes. Smoke include both initiators (polycyclic aromatic hydrocarbons such as benzopyrene and promoters, such as phenol derivatives.
2-Industrial Hazards. Certain industrial exposures increase the risk of developing lung cancer. All types of radiation may be carcinogenic. There was an increased incidence of lung cancer among survivors of the Hiroshima and Nagasaki atomic bomb blasts. Uranium is weakly radioactive, but lung cancer rates among nonsmoking uranium miners are 4 times higher than those of the general population, and among smoking miners they are about 10 times higher. The risk of lung cancer is increased with asbestos.
Lung cancer is the most frequent malignancy in persons exposed to asbestos, which has become a universally recognized carcinogen, particularly when coupled with smoking. Asbestos workers who do not smoke have a 5 times increased risk, and those who smoke have a 50 to 90 times greater risk of developing lung cancer than do nonsmoking control subjects.
3-Scarring. Some lung cancers arise in the vicinity of pulmonary scars and are termed scar cancers. Histologically, these tumors are usually adenocarcinomas. In most cases, the scar is a desmoplastic response to the tumor, but occasionally the scar has preceded the cancer. The scars incriminated are due to old infarcts, metallic foreign bodies, wounds, and granulomatous infections such as tuberculosis.
Classification. Numerous histologic classifications of bronchogenic carcinoma have been proposed, but the currently popular ones, based on classifications of the World Health Organization, divide these tumors into four major categories
1- Squamous cell carcinoma (25 to 40%)
2- Adenocarcinoma (25 to 40%)
3-Small cell carcinoma (20 to 25%)
4-Large cell carcinoma (10 to 15%) The incidence of adenocarcinoma has increased significantly in the last two decades, and it is now the most common form of lung cancer in women and, in many studies, men as well. There may be mixtures of histologic patterns, even in the same cancer.
Thus, combined types of squamous cell carcinoma and adenocarcinoma or of small cell and squamous cell carcinoma are not infrequent.
MORPHOLOGY. Bronchogenic carcinomas arise most often in and about the hilus of the lung. A small number of primary carcinomas of the lung arise in the periphery of the lung substance from the alveolar septal cells these are predominantly adenocarcinomas. Carcinoma of the lung begins as an a small area of thickening at bronchial mucosa. With progression, this small focus show appearance of an irregular, warty elevates or erodes the lining epithelium. The tumor may then follow a variety of paths. It may continue to fungate into the bronchial lumen to produce an intraluminal mass. It can also rapidly penetrate the wall of the bronchus to infiltrate along the peribronchial tissue into the adjacent region. In other instances, the tumor grows along a broad front to produce a cauliflower-like intraparenchymal mass. The neoplastic tissue is gray-white and firm to hard. Extension may occur to the pleural surface and then within the pleural cavity or into the pericardium. Spread to the tracheal, bronchial, and mediastinal nodes can be found in most cases. The frequency of nodal involvement varies slightly with the histologic pattern but averages greater than 50%. More distant spread of bronchogenic carcinoma occurs through both lymphatic and hematogenous pathways. the adrenals, for obscure reasons, are involved in more than half the cases. The liver (30 to 50%), brain (20%), and bone (20%) are additional favored sites of metastases.
• Squamous Cell Carcinoma. Squamous cell carcinoma is most commonly found in men and is closely correlated with a smoking history. The microscopic features are familiar in the form of production of keratin and intercellular bridges in the well-differentiated forms, but many less well differentiated squamous cell tumors are seen. This tumor arises in the larger, more central bronchi; tends to spread locally; and metastasizes somewhat later than the other patterns, but its rate of growth in its site of origin is usually more rapid than that of other types.
• Adenocarcinoma. Adenocarcinoma is the most common type of lung cancer in women and nonsmokers. The lesions are usually more peripherally located, tend to be smaller, and vary histologically from well-differentiated tumors with obvious glandular elements to papillary lesions resembling other papillary carcinomas, to solid masses with only occasional mucin-producing glands and cells.
• Small Cell Carcinoma. This highly malignant tumor has a distinctive cell type. The epithelial cells are generally small, have little cytoplasm, and are round or oval and, occasionally, lymphocyte like. It also called oat cell carcinomas. Small cell carcinomas have a strong relationship to cigarette smoking; only about 1% occur in nonsmokers. Most often hilar or central, they are the most aggressive of lung tumors, metastasize widely, and are virtually incurable by surgical means. They are the most common pattern associated with ectopic hormone production
• Large Cell Carcinoma. This anaplastic carcinoma has larger, more large cells and vesicular nuclei.
Clinical Course. Lung cancer is one of the most aggressive neoplasms, in the usual case, it is discovered in patients in their fifties whose symptoms are of approximately 7 months duration. The major presenting complaints are cough, weight loss, chest pain, and dyspnea. Increased sputum production is common and often contains diagnostic tumor cells when examined as cytologic specimens. Similarly, cytologic examination of a fine-needle aspirate of a tumor mass can often provide the diagnosis.
The overall 5-year survival rate is on the order of 9%. Despite this discouraging outlook, many patients have been cured by lobectomy or pneumonectomy, emphasizing the continued need for early diagnosis and adequate prompt therapy. Indeed, In the uncommon instance of localized solitary tumors less than 4 cm in diameter, surgical resection results in up to 40% 5-year survival for patients with squamous cell carcinoma and 30% for patients with adenocarcinoma and large cell carcinoma
المادة المعروضة اعلاه هي مدخل الى المحاضرة المرفوعة بواسطة استاذ(ة) المادة . وقد تبدو لك غير متكاملة . حيث يضع استاذ المادة في بعض الاحيان فقط الجزء الاول من المحاضرة من اجل الاطلاع على ما ستقوم بتحميله لاحقا . في نظام التعليم الالكتروني نوفر هذه الخدمة لكي نبقيك على اطلاع حول محتوى الملف الذي ستقوم بتحميله .
|