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Libros sobre el tema "Pulmonary Pathophysiology"

Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 19 de febrero de 2022

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1

Pulmonary pathophysiology. Philadelphia: Lippincott, 1995.

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2

Pulmonary pathophysiology: The essentials. 7a ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins, 2008.

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3

B, West John, ed. Pulmonary pathophysiology--the essentials. 4a ed. Baltimore: Williams & Wilkins, 1992.

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4

West, John B. (John Burnard), ed. Pulmonary pathophysiology: The essentials. 8a ed. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins Health, 2012.

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5

Pulmonary pathophysiology: The essentials. 3a ed. Baltimore: Williams & Wilkins, 1987.

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6

B, West John, ed. Pulmonary pathophysiology--the essentials. 5a ed. Baltimore, Md: Williams & Wilkins, 1998.

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7

Pulmonary pathophysiology: A clinical approach. 3a ed. New York: McGraw-Hill Medical, 2010.

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8

Workshop on "Chronic Pulmonary Hyperinflation" (1988 Montescano, Italy). Chronic pulmonary hyperinflation. London: Springer-Verlag, 1989.

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9

Pulmonary circulation: Diseases and their treatment. 3a ed. London: Hodder Arnold, 2011.

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10

Bittar, E. Edward. Pulmonary biology in health and disease. Editado por Springer-Verlag. New York: Springer, 2002.

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11

Belvisi, Maria G. y Jane A. Mitchell, eds. Nitric Oxide in Pulmonary Processes: Role in Physiology and Pathophysiology of Lung Disease. Basel: Birkhäuser Basel, 2000. http://dx.doi.org/10.1007/978-3-0348-8474-7.

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12

Workshop "Respiratory Muscles in C.O.P.D." (1986 Montescano, Italy). Respiratory muscles in chronic obstructive pulmonary disease. London: Springer-Verlag, 1987.

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13

Yuan, Jason X.-J., 1963- y Ward Jeremy P. T, eds. Membrane receptors, channels, and transporters in pulmonary circulation. Dordrecht: Springer, 2010.

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14

Principles of exercise testing and interpretation: Including pathophysiology and clinical applications. 5a ed. Philadelphia: Wolters Kluwer Health/Lippincott Williams & Wilkins, 2012.

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15

Die Wirkung skelettmuskulärer Aktivität auf den Atemwiderstand: Eine psychologische Untersuchung mit gesunden und asthmatischen Personen. Frankfurt am Main: P. Lang, 1996.

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16

West, John B. Pulmonary Pathophysiology: The Essentials (Pulmonary Pathophysiology). 7a ed. Lippincott Williams & Wilkins, 2007.

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17

Pulmonary Pathophysiology: The Essentials (Pulmonary Pathophysiology). 6a ed. Lippincott Williams & Wilkins, 2003.

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18

Juzar, Ali, Summer Warren R y Levitzky Michael G, eds. Pulmonary pathophysiology. New York: McGraw-Hill, Health Professions Division, 1999.

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19

Juzar, Ali, Summer Warren R y Levitzky Michael G, eds. Pulmonary pathophysiology. 2a ed. New York: Lange Medical Books/McGraw-Hill, 2005.

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20

Ali, Juzar. Pulmonary Pathophysiology. McGraw-Hill Professional, 1998.

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21

Ali, Juzar. Pulmonary Pathophysiology. McGraw-Hill Professional, 1998.

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22

Pulmonary Pathophysiology (The Pathophysiology Series). Fence Creek Publishing, 1998.

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23

West's Pulmonary Pathophysiology. Lippincott Williams & Wilkins, 2017.

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24

West, John Jr. Pulmonary Pathophysiology: The Essentials. 3a ed. Williams & Wilkins, 1987.

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25

Kenneth, Weir E. y Reeves John T, eds. Pulmonary vascular physiology and pathophysiology. New York: Dekker, 1989.

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26

Ali, Juzar, Warren G. Summer y Michael G. Levitzky. Pulmonary Pathophysiology (Lange Physiology Series). McGraw-Hill Medical, 2004.

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27

Ali, Juzar, Warren G. Summer y Michael G. Levitzky. Pulmonary Pathophysiology (Lange Physiology Series). 2a ed. McGraw-Hill Medical, 2004.

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28

J, Whipp Brian y Wasserman Karlman, eds. Exercise: Pulmonary physiology and pathophysiology. New York: M. Dekker, 1991.

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29

1925-, Morpurgo M., ed. Pathophysiology and treatment of pulmonary circulation. London: Springer-Verlag, 1988.

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30

Price, Laura y S. John Wort. Pathophysiology and causes of pulmonary hypertension. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0168.

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Pulmonary hypertension (PH) in the setting of critical illness may reflect the acute syndrome itself (such as acute massive pulmonary embolism or acute lung injury), and/or pre-existing ‘chronic’ causes of PH. To compound this, iatrogenic factors may also contribute to PH including the effects of positive pressure ventilation and certain vasoactive drugs. The presence of PH, especially when complicated by resulting right ventricular (RV) dysfunction and failure, is a poor prognostic feature in all settings. This chapter reviews the pathophysiology of acute PH in critical illness, and pre-existing chronic causes of PH, including acute decompensation in patients with pre-existing pulmonary arterial hypertension.
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31

Singer, Mervyn. Pathophysiology and causes of pulmonary embolism. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0170.

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Pulmonary embolus is predominantly due to thrombus breaking off from deep veins or from within the right heart, lodging within large or small vessels within the pulmonary vasculature, causing a variable degree of clinical features ranging from asymptomatic through to shock and cardiac arrest. Non-thrombotic causes include air or fat embolism. Outcome is predicated by the degree of right ventricular dysfunction. There are multiple risk factors including surgery, arrhythmias, prolonged immobility, venous stasis, pregnancy and an underlying pro-thrombotic tendency, either congenital or acquired. Numerous risk stratification scores have been developed derived from clinical features, imaging findings and biochemical markers of right ventricular strain and myocardial damage.
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32

F, Voelkel Norbert y Rounds Sharon 1946-, eds. The pulmonary endothelium. Chichester, West Sussex: John Wiley & Sons, 2009.

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33

A, Bray Michael y Anderson Wayne H, eds. Mediators of pulmonary inflammation. New York: M. Dekker, 1991.

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34

R, Filbin Michael, ed. Blueprints notes & cases, pathophysiology: Pulmonary, gastrointestinal, and rheumatology. Malden, Mass: Blackwell Pub., 2004.

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35

S, Zander Dani y Farver Carol F, eds. Pulmonary pathology. Philadelphia: Churchill Livingstone/Elsevier, 2008.

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36

Grassino, A. Chronic Pulmonary Hyperinflation. Springer, 2013.

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37

Grassino, A., C. Rampulla y R. Corsico. Chronic Pulmonary Hyperinflation. Springer, 2014.

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38

P, Lynch Joseph y DeRemee Richard A. 1933-, eds. Immunologically mediated pulmonary diseases. Philadelphia: Lippincott, 1991.

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39

Pulmonary Physiology and Pathophysiology: An Integrated, Case-Based Approach. Lippincott Williams & Wilkins, 2001.

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40

A, Parent Richard, ed. Treatise on pulmonary toxicology. Boca Raton: CRC Press, 1992.

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41

1926-, Grassi Carlo y Workshop "Update in Biochemistry of Pulmonary Emphysema" (1990 : Pavia, Italy), eds. Biochemistry of pulmonary emphysema. London: Springer-Verlag, 1992.

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42

Blanchard-Loeb. Heart Failure and Pulmonary Edema: Pathophysiology for Nurses Video Series. Delmar Learning, 2000.

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43

Vergnaud, Sophie, David Dobarro y John Wort. Pulmonary vasculature. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199657742.003.0017.

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A 16-year-old girl with a diagnosis of diffuse cutaneous systemic sclerosis is referred to a specialist pulmonary hypertension centre with a history of progressive breathlessness, reduced exercise tolerance, and raised pulmonary pressures on transthoracic echocardiogram. She is found to have pulmonary arterial hypertension on right cardiac catheterization and is started on sildenafil, a phosphodiesterase-5 inhibitor, which stabilizes her condition. An endothelin receptor antagonist is added, which provides some initial symptomatic improvement. She continues to deteriorate over a period of 5 years, ultimately requiring intravenous prostanoids, the only treatment to provide a real symptomatic and haemodynamic improvement. This chapter explores the physiology and pathophysiology of pulmonary arterial hypertension, its classification, the means of investigation and diagnosis, who to refer to specialist centres, and the concepts behind current and future treatment strategies.
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44

Textbook of pulmonary medicine. 2010.

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45

Tombetti, Enrico y Justin C. Mason. Pathophysiology of vasculitis. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755777.003.0017.

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Vasculitis represents a spectrum of disorders that are often divided on the basis of the predominant vessel size affected into large-, medium- and small-vessel vasculitides. This chapter will focus on the pathogenesis of the anti-neutrophil cytoplasmic antibody (ANCA)-associated medium- and small-vessel vasculitides (AAV), and large-vessel vasculitis, Takayasu arteritis, and giant cell arteritis. Underlying pathogenic mechanisms in vasculitis remain to be fully understood. In particular, the initiating event(s) are not known. A combination of infectious or other environmental triggers on a susceptible genetic background is currently favoured. In addition to the vessel size affected, the mechanisms of vascular injury vary. Moreover, extravascular granulomatosis may play an important role in disease manifestations. The innate and adaptive immune systems contribute to its pathogenesis. Although pathogenic antibodies have not been identified in large-vessel vasculitis, ANCA are directly implicated in small- and medium-vessel AAV. Disease manifestations are varied and diverse and may include arterial stenosis or aneurysms, glomerulonephritis and renal failure, gastro-intestinal, pulmonary, cutaneous, and neurological complications, visual disturbance, deafness, and nasal bridge collapse. Life-threatening cardiovascular disease is also seen, with myocarditis, pericarditis, valvular heart disease, thrombosis, systemic and pulmonary arterial hypertension, and accelerated coronary heart disease all reported. Despite this, the prognosis for patients with vasculitis has improved significantly in recent decades. Further understanding of the pathogenesis of vasculitis will lead to the discovery of further therapeutic targets and novel, safer biologic therapies.
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46

Denham, Ward, Dahan Albert y Teppema Luc J, eds. Pharmacology and pathophysiology of the control of breathing. Boca Raton, FL: Taylor & Francis, 2005.

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47

Pulmonary Vascular Physiology and Pathophysiology. Informa Healthcare, 1988.

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48

Modell, Jerome H. y Sean Kiley. Pathophysiology and management of drowning. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0348.

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Drowning is a process beginning with airway submergence under a fluid medium, progressing to aspiration, and ultimately death in the absence of intervention. Aspiration of both fresh- and saltwater can cause pulmonary oedema, decreased compliance, intrapulmonary shunting, and severe hypoxia. Devastating neurological injury resulting from prolonged cerebral hypoxia is proportional to the duration of submersion and delay in effective resuscitation and oxygenation. Victims presenting to the emergency department awake and alert, or even stuporous, are likely to have a good neurological outcome with follow-up intensive care. Those presenting comatose are much more likely to have severe neurological deficits. Keys to survival are: timely rescue from the water, immediate initiation of aggressive supportive care regarding airway, cardiovascular and pulmonary function, and optimization of tissue oxygenation.
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49

1952-, Müller B., Wichert P. von y International Symposium on Lung Surfactant (4th : 1992 : Marburg, Germany), eds. Lung surfactant: Basic research in the pathogenesis of lung disorders. Basel: Karger, 1994.

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50

Chronic pulmonary hyperinflation (Current topics in rehabilitation). Bi & Gi, 1991.

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