Pulmonary parenchyma

The definition above has replaced older ones that focused to varying degrees on chronic bronchitis and/ or emphysema. Chronic bronchitis and emphysema frequently represent different consequences of the same insult leading to changes in large aiiways, small airways and pulmonary parenchyma (Table 1). 

During occupational exposure, respiratory absorption of soluble and insoluble nickel compounds is the major route of entry, with gastrointestinal absorption secondary (WHO 1991). Inhalation exposure studies of nickel in humans and test animals show that nickel localizes in the lungs, with much lower levels in liver and kidneys (USPHS 1993). About half the inhaled nickel is deposited on bronchial mucosa and swept upward in mucous to be swallowed about 25% of the inhaled nickel is deposited in the pulmonary parenchyma (NAS 1975). The relative amount of inhaled nickel absorbed from the pulmonary tract is dependent on the chemical and physical properties of the nickel compound (USEPA 1986). Pulmonary absorption into the blood is greatest for nickel carbonyl vapor about half the inhaled amount is absorbed (USEPA 1980). Nickel in particulate matter is absorbed from the pulmonary tract to a lesser degree than nickel carbonyl however, smaller particles are absorbed more readily than larger ones (USEPA 1980). Large nickel particles (>2 pm in diameter) are deposited in the upper respiratory tract smaller particles tend to enter the lower respiratory tract. In humans, 35% of the inhaled nickel is absorbed into the blood from the respiratory tract the remainder is either swallowed or expectorated. Soluble nickel compounds... 

An appreciable body of evidence has accumulated to indicate that ozone has extrapulmonary effects. Although some of the reported effects may be secondary to the reaction of ozone with intrapulmonary neural receptors or to release of humoral substances from the lung, other finding appear to be mote directly related to an oxidizing effect of ozone. The biochemical basis for the latter is unclear, particularly because the reactivity of ozone and its short-lived intermediates would make it unlikely for them to penetrate the pulmonary parenchyma. Earlier studies on the subject of extrapulmonary effects have been reviewed by Stokinger. ... 

No degenerative changes in the pulmonary parenchyma were found, but 7/20 mice that died 15 months after intravenous injection of Thorotrast (Guimaraes et al. 1955) and 8/20 mice that were sacrificed 5-12 months after injection of Thorotrast (Guimaraes and Lamerton 1956) had lung adenomas. There was no significant difference in survival between the treated and control animals in either study. In a few cases, an association between the presence of Thorotrast deposits in the lungs and the proliferation of bronchioles and alveoli was found. 

Tumor colonies that are not pigmented and are minimally different in their color from the pulmonary parenchyma are more difficult to enumerate. The following method is one of several that can be used to induce contrast between tumor colonies and lung parenchyma. 

Pinkerton KE, Plopper CG, Mercer RR, et al. 1986. Airway branching patterns influence asbestos fiber location and the extent of tissue injury in the pulmonary parenchyma. Lab Invest 55 688-695. 

For an evaluation of the pulmonary parenchyma, a native scan without contrast media is sufficient due to the good natural contrast between air and soft tissue structures. But for evaluating mediastinal structures such as lymph nodes, the heart or the pulmonary vessels, i.v. contrast medium should be administered in order to enhance the contrast of the soft tissue structures. 

The uncontrolled generation of superoxide and H2O2 might immediately cause damage to pulmonary parenchyma. 

The primary alteration of the respiratory tract of patients with cystic fibrosis is the hypersecretion of mucus. It is not known whether the mucus is normal or contains excessive amounts of electrolytes. In any case, the mucus secretion is not properly evacuated. It first occludes the smaller bronchi. If the occlusion is incomplete, the alveoli become distended, the inspired air cannot be expired, and emphysematous blebs develop. If the obstruction is complete, atelectasis occurs. The changes in the bronchi and the pulmonary parenchyma favor infection, especially by staphylococci. Pulmonary abscesses, bronchial pneumonia, bronchitis, and pneumonia develop in fact, children with cystic fibrosis often die from respiratory infection. Pneumothorax, hemoptysis, and emphysema are rare complications of the pulmonary disturbance observed in cystic fibrosis (see Fig. 4-46). 

Pretreatment CT of the chest is a key examination for determining the number, size, and location of the lesions. Their relationship to the heart, major bronchi and vessels has to be evaluated, as well as the status of the surrounding pulmonary parenchyma. Furthermore it constitutes the term of reference for post-treatment follow-up studies. 

The multicenttic variant is characterized by numerous germinal centers, with an interfollicular stroma rich in plasma cells and small vessels. In this variant, the pulmonary parenchyma can also rarely show an associated lymphocytic interstitial pneumonia that is rich in CD138 (syndecan-l)-positive plasma cells (26,110). HHV-8 DNA is often detected in biopsies of lymph nodes from patients with multicentric Castleman disease (27,101,111). There is an interesting report of two patients who had both primary pulmonary hypertension and Castleman disease of these, one had HHV-8 demonstrated in lung tissue (and specifically in the plexiform lesions) (112). 

Fig. 7.11. Prone inspiratory thin-section computed tomography of an asbestos miner showing areas of differing attenuation with regions of pulmonary parenchyma which appear blacker than adjacent areas (arrows), an indirect sign of small airways disease. The difference may be accentuated on end-expiratory sections (not shown)...

T2 Each ipsilateral pleural surface At least one of the following (a) involvement of the diaphragmatic muscle or (b) a confluent visceral pleural tumor (including fissures) or tumor extension from the visceral pleura into the underlying pulmonary parenchyma... 

Terzidis-Trabelsi, H., Pilatte, Y., Greffard, A., Bignon, J., and Lambre, C., 1991, Sialidase in the guinea pig pulmonary parenchyma Increased activity in the cytosolic and microsomal subcellular fractions after stimulation with bacillus Calmette Guerin, Biol. Chem. Hoppe-Seyler 372 437-442. 

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