Crofton and Douglas's Respiratory Diseases by Anthony Seaton, A. Gordon Leitch, Douglas Seaton

By Anthony Seaton, A. Gordon Leitch, Douglas Seaton

Now in its 5th variation, Crofton and Douglas's breathing ailments has firmly tested itself because the best medical textbook on illnesses of the chest.

Presented, for the 1st time, as a two-volume set, this vintage textual content has been thoroughly rewritten and significantly extended. wide revisions make sure that those volumes current an up to date overview of all points of lung disease

. The contributions of a few 18 prime specialists make sure that every one zone is comprehensively lined and new to this version are chapters at the genetics of lung ailment, smoking, pollution, sleep apnoea, diving, lung transplantation and medico-legal elements. The alterations in content material replicate the velocity of swap within the parts involved not just by way of realizing of the disorder techniques but additionally their remedy. the only bankruptcy on bronchial asthma that seemed in earlier versions, has now been multiplied into 3 chapters masking epidemiology, mechanisms and administration, reflecting the large examine attempt at the moment underway following a marked bring up within the occurrence of this ailment in fresh years.

This new version maintains to supply an outstanding reference either for the trainee and expert in breathing drugs, in addition to the final health professional. it is going to be super worthy at the ward and within the place of work, the place scientific difficulties come up and questions are requested which desire transparent solutions.

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Sample text

In disease, a large physiological dead space (wasted ventilation) represents an increase in the popula. tion of alveoli with high VA/Q ratios; a large physiological shunt represents an increase in the population of alveoli . with low VA/Q ratios. 0 Ventilation–perfusion ratio Fig. 13 Distribution of ventilation–perfusion ratios measured by the multiple inert gas technique in a normal subject (a) and in a patient with chronic bronchitis and emphysema (b). ) embolism [40] the associated hypoxaemia can be shown to be due to excessive shunt, although the mechanisms underlying this are unclear.

Am Rev Respir Dis 1966; 93: 1. 50 Van As A, Webster I. The organisation of ciliary activity and mucus transport in pulmonary airways. S Afr Med J 1972; 146: 347. 51 Sleigh MA. The nature and action of respiratory tract cilia. In: Brain D, Proctor DF, Reid LM, eds. Respiratory Defense Mechanisms Part I. New York: Marcel Dekker, 1977. 52 Afzelius BA, Mossberg B. Thorax 1980; 35: 401. 53 Olivieri D, Foresi A. Airway inflammation in asthma. Curr Opin Pulm Med 1995; 1: 31. 54 Mangan A, Frachon I, Rain B et al.

Scientific Basis of Respiratory Medicine. London: Heinemann, 1977. 102 Gross NJ. Pulmonary surfactant: unanswered questions. Thorax 1995; 50: 325. 103 Hills BA. What is the true role of surfactant in the lung? Thorax 1981; 36: 1. 104 Hills BA. What forces keep the air spaces of the lung dry? Thorax 1982; 37: 713. 105 Bensch K, Schaefer K, Avery ME. Granular pneumocytes: electron microscopic evidence of their exocrine function. Science 1984; 145: 1318. 106 Wright JR, Clements JA. Metabolism and turnover of lung surfactant.

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