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الكلية كلية طب الاسنان
القسم العلوم الاساسية
المرحلة 3
أستاذ المادة علي زكي ناجي الاسدي
5/31/2011 7:50:03 AM
emphysema
emphysema is a condition of the lung characterized by permanent enlargement of the airspaces distal to the terminal bronchiole, accompanied by destruction of their walls, in contrast, the enlargement of airspaces unaccompanied by destruction is termed over-inflation.
types of emphysema. emphysema is defined in terms of the anatomic nature of the lesion, it can be classified according to its anatomic distribution within the lobule into major types:
(1) centriacinar,
(2) panacinar,
(3) others. of these, only the first two cause clinically significant airflow obstruction.
centriacinar emphysema is far more common than the panacinar form, constituting greater than 95% of cases. centriacinar (centrilobular emphysema). the distinctive feature of this type of emphysema is the pattern of involvement of the lobules the central or proximal parts of the acini, formed by respiratory bronchioles, are affected, whereas distal alveoli are spared. thus, both emphysematous and normal airspaces exist within the same acinus and lobule. the lesions are more common and usually more severe in the upper lobes, particularly in the apical segments. the walls of the emphysematous spaces often contain large amounts of black pigment. inflammation around bronchi and bronchioles and in the septa is common.
centriacinar emphysema occurs predominantly in heavy smokers, often in association with chronic bronchitis. in addition, some lesions of so-called coal workers pneumoconiosis bear a striking resemblance to centriacinar emphysema. these points suggest an important role for tobacco products and coal dust in the genesis of this type of emphysema. panacinar (panlobular) emphysema. in this type, the acini are uniformly enlarged from the level of the respiratory bronchiole to the terminal blind alveoli .the prefix pan- refers to the entire acinus but not to the entire lung. in contrast to centriacinar emphysema, panacinar emphysema tends to occur more commonly in the lower zones and it is usually most severe at the bases. this type of emphysema is associated with alpha1 - antitrypsin (alpha1 -at) deficiency incidence. emphysema is a common disease. 50% combined incidence of panacinar and centriacinar emphysema at autopsy, and the pulmonary disease was considered to be responsible for death in 6.5% of these patients .there is a clear-cut association between heavy cigarette smoking and emphysema, and the most severe type occurs in men who smoke heavily. pathogenesis. the most important hypothesis to account for the destruction of alveolar walls is the protease-antiprotease mechanism. this hypothesis is based on two important observations, one clinical and one experimental. the first is that homozygous patients with a genetic deficiency of the protease inhibitor alpha1 -at have a markedly enhanced tendency to develop pulmonary emphysema, which is compounded by smoking. alpha1 -at (which is present in serum, tissue fluids, and macrophages) is a major inhibitor of proteases, particularly elastase, secreted by neutrophils during inflammation. the protease-antiprotease theory holds that alveolar wall destruction results from an imbalance between proteases (mainly elastase) and antiproteases in the lung. the principal cellular elastase activity is derived from neutrophils . neutrophil elastase is capable of digesting human lung, and this digestion can be inhibited by alpha1 -at. such elastase induces emphysema when instilled into the trachea of experimental animals. thus, the following sequence is postulated to explain the effect of alpha1 -at deficiency on the lung: neutrophils are normally sequestered in the lung (more in the lower zones than in the upper), and a few gain access to the alveolar space. any stimulus that increases either the number of leukocytes (neutrophils and macrophages) in the lung or the release of their elastase-containing granules increases elastolytic activity. stimulated neutrophils also release oxygen free radicals, which also inhibit alpha1 -at activity. thus, emphysema is seen to result from the destructive effect of high protease activity in subjects with low antiprotease activity. the protease-antiprotease hypothesis also explains the deletingrious effect of cigarette smoking because both increased elastase availability and decreased antielastase activity occur in smokers smokers have greater numbers of neutrophils and macrophages in their alveoli. the increased recruitment of neutrophils into the lung is likely to result, in part, from the release by activated alveolar macrophages of neutrophil chemotactic factors this release being stimulated by smoking. in addition, nicotine is chemotactic for neutrophils. smoking stimulates release of elastase from neutrophils. smoking enhances elastolytic protease activity in macrophages. oxidants in cigarette smoke and oxygen free radicals secreted by neutrophils inhibit alpha1 -at and thus decrease net antielastase activity in smokers. it is thus postulated that impaction of smoke particles in the small bronchi and bronchioles, with the resultant influx of neutrophils and macrophages and increased elastase and decreased alpha1 -at activity, causes the centriacinar emphysema seen in smokers. in contrast, it is postulated that the panacinar emphysema of alpha1 -at-deficient individuals reflects total lack of antiprotease throughout the acinus and susceptibility to chronic low-level proteolysis from neutrophils in transit through the lung circulation. the predominantly lower lung distribution (where perfusion and neutrophil numbers are greatest) of panacinar emphysema is also consistent with this postulate.
morphology. panacinar emphysema produces voluminous lungs, often overlapping the heart and hiding it when the anterior chest wall is removed. the macroscopic features of centriacinar emphysema are less impressive. the lungs may not appear particularly pale or voluminous unless the disease is well advanced. microscopic examination show complete destruction of septal walls, and the distribution of damage within the pulmonary lobule. with advance of the disease, adjacent alveoli fuse, producing even larger abnormal airspaces and possibly blebs or bullae. as mentioned, there may or may not be evidence of bronchitis or bronchiolitis.
other types of emphysema.
compensatory emphysema (hyperinflation) the term compensatory emphysema is sometimes used to designate dilation of alveoli but not destruction of septal walls in response to loss of lung substance elsewhere. it is best exemplified by the hyperexpansion of the residual lung parenchyma that follows surgical removal of a diseased lung or lobe.
senile emphysema. senile emphysema refers to the over-distended, sometimes voluminous lungs found in the aged. these changes result from age-related alterations of the internal geometry of the lung larger alveolar ducts and smaller alveoli that occur without loss of elastic tissue or destruction of lung substance.
obstructive over-inflation. obstructive overinflation refers to the condition in which the lung expands because air is trapped within it. a common cause is subtotal obstruction by a tumor or foreign object.
bullous emphysema. bullous emphysema refers merely to any form of emphysema that produces large subpleural blebs or bullae (spaces > 1 cm in diameter in the distended state). on occasion, rupture of the bullae may give rise to pneumothorax.
bronchial asthma asthma is a chronic relapsing inflammatory disorder characterized by hyper-reactive airways, leading to episodic, reversible broncho-constriction, owing to increased responsiveness of the tracheobronchial tree to various stimuli. most asthma is associated with atopy, which represents increased susceptibility to generate immunoglobulin e (ige) in response to external allergens those develop attacks of severe dyspnea, coughing, and wheezing triggered by sudden episodes of bronchospasm. between the attacks, patients may be virtually asymptomatic. rarely a state of unremitting attacks (status asthmaticus) proves fatal usually such patients have had a long history of asthma.
asthma has traditionally been divided into two basic types extrinsic and intrinsic types.
extrinsic asthma: is initiated by a type i hypersensitivity reaction induced by exposure to an extrinsic antigen. subtypes include atopic (allergic) asthma, occupational asthma, and allergic bronchopulmonary aspergillosis.
intrinsic asthma: is initiated non-immune mechanisms, including ingestion of aspirin pulmonary infections, especially viral cold inhaled irritants stress and exercise. increased airway hyperreactivity is also more likely to manifest bronchospasm after exposure to one of the agents associated with intrinsic asthma. pathogenesis. atopic asthma. this most common type of asthma usually begins in childhood.
the disease is triggered by environmental antigens, such as dusts, pollens, animal dander, and foods. a positive family history of atopy is common, and asthmatic attacks are often preceded by allergic rhinitis, urticaria, or eczema. skin test with the offending antigen in these patients results in an immediate wheal-and-flare reaction, a classic example of type i ige-mediated hypersensitivity reaction,. in the airways, the scene for the reaction is caused by initial sensitization to inhaled antigens (allergens), which stimulate induction of t cells, which release cytokines, these cytokines, in turn, promote ige production by b cells, growth of mast cells, and growth and activation of eosinophils. recall that exposure of presensitized ige-coated mast cells to the same or a cross-reacting antigen stimulates cross-linking of ige and the release of chemical mediators. the antigens, sensitized mast cells on the mucosal surface and subepithelial surface provokes bronchoconstriction. this occurs within minutes after stimulation and is called the acute, or immediate, response, which consists of bronchoconstriction, edema, mucus secretion. mast cells also release cytokines that cause the influx of other leukocytes, including neutrophils and monocytes, lymphocytes, basophils, and particularly eosinophils (il-5). these inflammatory cells set the stage for the late-phase reaction, which starts 4 to 8 hours later and may persist for 12 to 24 hours or more nonatopic asthma. the second large group is the non-atopic, which is most frequently triggered by respiratory tract infection. viruses . a positive family history is uncommon, serum ige levels are normal, and there are no other associated allergies. in these patients, skin test results are usually negative, and although hypersensitivity to microbial antigens may play a role, present theories place more stress on hyperirritability of the bronchial tree. it is thought that virus-induced inflammation of the respiratory mucosa lowers the threshold of the subepithelial vagal receptors to irritants. inhaled air pollutants, such as sulfur dioxide, ozone, and nitrogen dioxide, may also contribute to the chronic airway inflammation and hyperreactivity present in some cases.
morphology of asthma.
grossly the lungs are overdistended because of overinflation, and there may be small areas of atelectasis. the most striking macroscopic finding is occlusion of bronchi and bronchioles by thick, mucous plugs.
histologically the mucous plugs contain whorls of shed epithelium, which give rise to the well-known curschmann spirals. numerous eosinophils and charcot-leyden crystals are present the latter are collections of crystalloid made up of eosinophil membrane protein.
the other characteristic histologic findings of asthma include thickening of the basement membrane of the bronchial epithelium edema and an inflammatory infiltrate in the bronchial walls, with a prominence of eosinophils, which form 5 to 50% of the cellular infiltrate an increase in size of the submucosal glands hypertrophy of the bronchial wall muscle, a reflection of prolonged bronchoconstriction
clinical course. the classic asthmatic attack lasts up to several hours and is followed by prolonged coughing the raising of copious mucous secretions provides considerable relief of the respiratory difficulty. in some patients, these symptoms persist at a low level all the time. in its most severe form, status asthmaticus, the severe acute paroxysm persists for days and even weeks, and, under these circumstances, ventilatory function may be so impaired as to cause severe cyanosis and even death. the clinical diagnosis is aided by the demonstration of an elevated eosinophil count in the peripheral blood and the finding of eosinophils, curschmann spirals, and charcot-leyden crystals in the sputum. in the usual case, with intervals of freedom from respiratory difficulty, the disease is more discouraging and disabling than lethal. with appropriate therapy to relieve the attacks, patients with asthma are able to maintain a productive life. occasionally the disease disappears spontaneously. in the more severe forms, the progressive hyperinflation may eventually produce emphysema. superimposed bacterial infections may lead to chronic persistent bronchitis, bronchiectasis, or pneumonia. in some cases, cor pulmonale and heart failure eventually develop.
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 .
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