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Encyclopedia of respiratory medicine PDF

2401 Pages·2019·41.38 MB·english
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INTRODUCTION R espiratorydiseasesrepresentoneofthelargesthealthproblemswordwide.Diseasessuchasasthmaand the smokingrelated diseases are alreadycommonand increasingsowe urgentlyneedbetterapproaches totreatorcurethesediseases.Atthesametime,newrespiratorydiseasessuchasthoseassociatedwithviruses threaten pandemics that challenge our national health systems. Withthesecontinuedchallengesfornewtreatmentwithbetterpatientcare,clinicalandrespiratoryresearchers have sought better approaches to all aspects of patient care from improved diagnoses to superior therapies. This has lead to an explosion of new research with an increasingly better understanding of how to diagnose diseases and then develop new therapies. Thus, for example ever improving technologies for imaging lung disease have lead to increasingly better diagnoses, although challenges remain as we seek to further improve resolution. At the same time, the revolution in molecular biology, culminating with the publication of the completehumangenome,hasleadtohopesforfindingmoreprecisecluestodiseasesusceptibilitypathogenesis in genetic analysis. This is leading to new concepts in pharmacogenomics as we start to use new drugs, including those used for lung cancers, being directed at mutations associated with disease. ThisisthefirstEncyclopaediaofRespiratoryMedicine.Itisourhopethatitiscomprehensiveandcaptures the key aspects of current patient care, as well as the exciting developments in respiratory science that we all believe will eventually lead to better patient care in the twenty first century. This encyclopaediaiscomprehensive inscopeandprovidesclinicianandresearcherwithasnapshotofthe current state of knowledge in respiratory medicine. All entries have adhered to a structured layout, starting withanabstractcrystallizingthekeyfactsandfinishingwithreadinglistsforthosewhowanttodelvefurther intothesubject.Inaddition,mostentrieshaveacolourdiagramdesignedtohelpunderstandingandprovidea valuable aid for undergraduate and post-graduate teaching. Theseareexcitingtimesforrespiratorymedicine.Wehopethisencyclopediawillbecomeavalubletoolfor clinicians and researches at all stages of their careers from those beginning their carreers to those established but wanting to update themselves on the new developments. Finally,wewouldliketothankourAdvisoryEditorialBoardwhohelpedsomuchinshapingthecontentsof this works, as well as the authors who wrote the articles and faced the challenge of condensing areas of respiratory medicine, often the subject of entire textbooks, into a short article of 4000 words or less. GEOFFREY J. LAURENT STEVEN D. SHAPIRO FOREWORD Animalslivebytwoprincipalthings,foodandbreath.Ofthese,byfarthemostimportantistherespiration,forifitisstopped,theman willnotendurelong,butimmediatelydies.–AretaeustheCappocian(150–200AD) O f course, not all medical specialists would agree with this statement, and those who disagree would be quick to posit that it is the failure of ‘‘their’’ particular organ that tends to cause immediate death. However,thatisnottheissue.Thepointofthisquotationistoillustratethattheproperfunctioningofthelung has been a subject of great interest for centuries. The Greek physician Aretaeus devoted many of his observations to diabetes, but his manuscript ‘‘On the Causes and Indications of Acute and Chronic Diseases’’ also discussed lung diseases, such as pneumonia. Since his time, great numbers of physicians from all conti- nents and cultures have contributed to our knowledge of respiratory diseases. While acknowledging our rich history of discoveries about pulmonary and respiratory medicine— dis- coveries that were made by men and women whose names symbolize the great journey of this specialty—one must concede that the field experiencedanextraordinarygrowthspurt beginninginthe 1940s.Knowledgeof respiratory physiology, which developed very fast during World War II, created a tidal wave of interest that continued for years afterward. The ability to measure and understand respiratory physiology and its alter- ations became a diagnostic tool, and it opened the door to therapeutic or respiratory support procedures. But, then, in the 1950s and 1960s cell biology and subcellular research entered the scene. The potential of molecular biology and genetics was quickly recognized, and respiratory medicine appreciated that a better un- derstanding of normal and disordered biological respiratory processes hinged on use of these new approaches. Lung and respiratory researchers, impelled in part by the ever-increasing public health burdens of respiratory diseases, seized the opportunity. The stage was set for progress to occur. The architects of this ‘‘revolution’’ in respiratory medicine are well known; it is our good fortune that many have contributed to these four volumes. Four volumes! y Encyclopedia! y Indeed, these four volumes truly constitute an encyclopedia of pulmo- nary biology and respiratory medicine! Respiratorymedicineisstillgrowing.Becauseitissuchadynamicandexcitingfield,newinvestigatorswill almost surely want to be part of it. However, to do so they will need to know about the established state of knowledge that will be the basis of their work. New investigators in the science of respiratory medicine, whetherinterestedinfundamentalresearchorclinicalresearchorapplication,willfindideasandinspirationin these volumes. All of the tools of the trade are assembled therein. Asnoted,respiratorymedicinehasbeenaprogressiveandexpandingfieldbut,asisthecasewithmanyfields of medicine, the transfer of what we know to the general practice of medicine has been slow and limited. Translation, as it is called, is an emerging discipline in need of assistance; fortunately, the breadth of the knowledge presented in these volumes provides tools to facilitate this translation process. Thisfour-volumeencyclopediais,atonce,bothatributetothecenturiesofpioneeringinvestigationsinthe fieldofrespiratorymedicineandafoundationforevengreateraccomplishmentsinthefuture.Thepresentation ofallthisknowledgeintheseexcellentandcomprehensivevolumescanonlyservetostimulatefurtherworkof equal or surpassing significance. The editors and the authors are to be commended for their contributions to this singular effort. Because of their work, respiratory science and medicine will advance faster and patients worldwide will be the beneficiaries. Claude Lenfant, MD Gaithersburg, Maryland Notes on the Subject Index To save space in the index, the following abbreviations have been used: ALI acute lung injury ARDS acute respiratory distress syndrome BAL bronchoalveolar lavage BPD bronchopulmonary dysplasia CAP community-acquired pneumonia CFTR cystic fibrosis transporter regulation COP cryptogenic organizing pneumonia COPD chronic obstructive pulmonary disease CWP coal workers’ pneumoconiosis G-CSF granulocyte colony-stimulating factor GERD gastroesophageal reflux disease GM-CSF granulocyte-macrophage colony-stimulating factor HUVS hypocomplementemic urticarial vasculitis syndrome IL interleukin IPF idiopathic pulmonary fibrosis IPH idiopathic pulmonary hemosiderosis MCP monocyte chemoattractant protein M-CSF macrophage colony-stimulating factor MIP macrophage inflammatory protein MMP matrix metalloproteinase NSCLC non-small cell lung carcinoma PPAR peroxisome proliferator-activated receptor SCLC small-cell lung carcinoma SP surfactant protein TGF transforming growth factor TIMP tissue inhibitor of metalloproteinases TNF tumor necrosis factor VEGF vascular endothelial growth factor Editorial Advisory Board Kenneth B. Adler, North Carolina State University, Raleigh, NC, USA Peter J. Barnes, Imperial College London, UK Paul Borm, Zuyd University, Heerlen, The Netherlands Arnold R. Brody, Tulane Medical School, New Orleans, LA, USA Rachel C. Chambers, University College London, UK Augustine M. K. Choi, University of Pittsburgh, PA, USA Jack A. Elias, Yale University School of Medicine, New Haven, CT, USA Patricia W. Finn, University of California San Diego, La Jolla, CA, USA Stephen T. Holgate, University of Southampton, Southampton, UK Steven Idell, The University of Texas Health Center at Tyler, TX, USA Sebastian L. Johnston, National Heart and Lung Institute, Imperial college London, UK Talmadge E. King, Jr, University of California, San Francisco, CA, USA Stella Kourembanas, Children’s Hospital Boston, Harvard Medical School, Boston, MA, USA Y. C. Gary Lee, University College London, UK Richard Marshall, University College London, UK Sadis Matalon, University of Alabama, Birmingham, AL, USA Joel Moss, National Institutes of Health, Bethesda, MD, USA William C. Parks, University of Washington, Seattle, WA, USA Charles G. Plopper, University of California, Davis, CA, USA Bruce W. S. Robinson, The University of Western Australia, Nedlands, Australia Neil Schluger, Columbia University College of Physicians and Surgeons, New York, NY, USA Edwin K. Silverman, Brigham and Women’s Hospital Boston, MA, USA Eric S. Silverman, Brigham and Women’s Hospital, Boston, MA, USA Peter Sly, Institute for Child Health Research, West Perth, Australia Kingman Strohl, Case Western Reserve University, Cleveland, OH, USA Teresa D. Tetley, Imperial College London, UK John B. West, University of California, San Diego, CA, USA Editors Geoffrey J Laurent, Royal Free and University College Medical School, London, UK Steven D Shapiro, Brigham and Woman’s Hospital, Boston, USA Dedication To my family, Lal, Guy, David and Gabrielle (GJL). MycontributiontothisworkwouldnothavebeenpossiblewithouttheloveandsupportfrommywifeNicole and my daughters Calli, Tess, Skylar, and Ellery. I also thank my mentors and trainees for my continual education and theDivision ofPulmonary andCriticalCare Medicine atBrigham and Women’s Hospital who took care of our patients allowing me the time to undertake this project (SDS) Permission Acknowledgments The following material is reproduced with kind permission of Lippincott Williams and Wilkins Figure 4 and 8 of ARTERIAL BLOOD GASES Table 1 of ARTERIES AND VEINS Figure 2 and 3 of BREATHING | Breathing in the Newborn Figure 2a, 2b, 3, 4 and 5 of DRUG-INDUCED PULMONARY DISEASE Table 1, 2 and 3 of DRUG-INDUCED PULMONARY DISEASE Figure 2 of ENVIRONMENTAL POLLUTANTS | Diesel exhaust particles Figure 4 of EXERCISE PHYSIOLOGY Figure 2 of FLUID BALANCE IN THE LUNG Figure 2 of GASTROESOPHAGEAL REFLUX Figure 2 of GENE REGULATION Figure 2 of HIGH ALTITUDE, PHYSIOLOGYAND DISEASES Figure 2 and 3 of IDIOPATHIC PULMONARY HEMOSIDEROSIS Table 1 of IDIOPATHIC PULMONARY HEMOSIDEROSIS Figure 1, 2 and 3 of OXYGEN-HEMOGLOBIN DISSOCIATION CURVE Figure 10a, 10b and 11a of SYSTEMIC DISEASE | Eosinophilic Lung Diseases http://www.lww.com The following material is reproduced with kind permission of Nature Publishing Group Figure 2 of COAGULATION CASCADE | iuPA, tPA, uPAR Figure 1 of COAGULATION CASCADE | Tissue Factor Figure 1a of MATRIX METALLOPROTEINASES Figure 1 of MYOFIBROBLASTS 2 Figure 1 of VESICULAR TRAFFICKING http://www.nature.com/nature and http://www.nature.com/reviews The following material is reproduced with kind permission of Taylor & Francis Ltd Figure 2 of AUTOANTIBODIES Table 1 of BASAL CELLS Figure 1 of NEUROPHYSIOLOGY | Neuroendocrine Cells Table 1 of NEUROPHYSIOLOGY | Neuroendocrine Cells Figure 1 and 2 of SURFACANT | Overview Tables 1, 2, 3 and 4 of SURFACANT | Overview http://www.tandf.co.uk/journals A ACETYLCHOLINE J Zaagsmaand HMeurs,Universityof Groningen, vagosympathetic trunk; when applied to a second, Groningen, TheNetherlands unstimulated heart, the perfusate slowed its rate, &2006ElsevierLtd.Allrightsreserved. resembling the effect of vagus stimulation. In 1926 Loewi provided evidence for identification of Vagusstoff as acetylcholine. Acetylcholine is the Abstract neurotransmitter of all sympathetic and parasympa- Intheairways,acetylcholineisaneurotransmitterinparasym- thetic autonomic ganglia and of the postganglionic patheticgangliaandinpostganglionicparasympatheticnerves, parasympatheticnerves.Intheairways,theparasym- aswellasanonneuralparacrinemediatorinvariouscellsinthe patheticgangliaarelocatednearorwithintheairway airwaywall.Ganglionictransmissionbyacetylcholineismedi- wall. Ganglionic transmission mediated by acetyl- atedbynicotinicreceptors,whichareligand-gatedinchannels, whereaspostganglionictransmissionisthroughG-protein-cou- cholineisthroughnicotinicreceptorswhichbelongto pled muscarinic receptors. Of the five mammalian muscarinic the family of ligand-gated ion channels. Postgan- receptor subtypes, mainly M1, M2, and M3 receptors are in- glionic transmission by acetylcholine, released from volvedinairwayfunctions.G -coupledM receptorsfacilitate q 1 parasympathetic nerve terminals, is through mu- ganglionic transmission mediated by nicotinic receptors and scarinic receptors of which five different subtypes modulatesurfactantproduction andfluid resorption in theal- veoli. Prejunctional G -coupled M receptors in parasympa- have been identified, all being G-protein-coupled i/o 2 theticnerveterminalsattenuateacetylcholinereleaseuponnerve receptors. During periods of airway inflammation stimulation.M2receptorsarealsoabundantlypresentinairway vagal release of acetylcholine may be increased by smoothmuscle;however,themajorfunctionofthesepostjunct- various mechanisms. Hence, both in asthma and ionalM receptorsisunknown.PostjunctionalG -coupledM 2 q 3 (particularly) in chronic obstructive pulmonary dis- receptorsmediateairwaysmoothmusclecontractionandmucus secretion.DysfunctionoftheprejunctionalM autoreceptorin- ease (COPD) blockade of postjunctional muscarinic 2 ducedbyallergicairwayinflammationhasbeenimpliedinex- receptors is the key to reversing airway obstructions. aggeratedvagalreflexactivityandairwayhyperresponsiveness in asthma. Inflammation-induced increased M receptor stim- 3 ulation may be involved in airway remodeling in chronic Synthesis, Storage, and Release asthma. Possible mechanisms include potentiation of growth factor-inducedproliferationofairwaysmoothmusclecellsand Acetylcholine is synthesized from choline and acetyl- inductionofacontractilephenotypeofthesecells.Exaggerated coenzyme A (acetyl-CoA) in the cytoplasm of the M receptor stimulation may also cause reduced responsive- 3 ness to b -adrenoceptor agonists by transductional cross-talk nerve terminal through the enzyme choline acetyl- 2 between phosphoinositide metabolism and adenylyl cyclase, transferase (ChAT). Choline is taken up by the nerve whichinvolvesproteinkinaseC-induceduncouplingoftheb2- terminal from the extracellular fluid through a so- adrenoceptorfromtheeffectorsystem.Muscarinicreceptoran- dium-dependent carrier; this transport is the rate- tagonistshavebeenshowntobeeffectiveinairwaydiseaseslike limitingprocessinacetylcholinesynthesis.Acetyl-CoA asthmaand,especially,chronicobstructivepulmonarydisease. is synthesized in mitochondria which are abundantly Of these, tiotropium bromide is particularly useful, due to its longdurationofactionaswellasitskineticselectivityforthe present in the nerve endings. Most of the synthesized M3receptor. acetylcholine is actively transported from the cytosol into synaptic vesicles by a specific transporter; this vesicular (‘quantal’) package of acetylcholine reaches Introduction up to 50000molecules per vesicle. Acetylcholineisaneurotransmitterinthecentraland Release of acetylcholine is initiated by influx of peripheralnervoussystemwhereitplaysamajorrole Ca2þ ionsthroughvoltage-operatedN-orP-typecal- in the afferent neurons of both the autonomic cium channels. The increased intracellular Ca2þ ions and somatic (voluntary) branches. As a chemical bind to a vesicle-associated protein (synaptotagmin) transmitter, it has been identified as ‘Vagusstoff’ in which favors association of a second vesicle protein 1921 by Otto Loewi showing its release from (synaptobrevin) with one or more proteins in the an isolated frog heart following stimulation of the plasma membrane of the nerve terminal. Following

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