Thematische Bibliographien / Pulmonary Pathophysiology / Zeitschriftenartikel
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Zeitschriftenartikel zum Thema „Pulmonary Pathophysiology“

Autor: Grafiati
Veröffentlicht am 4. Juni 2021
Zuletzt aktualisiert am 19. Februar 2022

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1

Cherniack, Neil S. „Pulmonary Pathophysiology“. Annals of Internal Medicine 131, Nr. 5 (07.09.1999): 399. http://dx.doi.org/10.7326/0003-4819-131-5-199909070-00022.

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2

Gonzalez, Norberto C. „PULMONARY PATHOPHYSIOLOGY“. Shock 11, Nr. 2 (Februar 1999): 152. http://dx.doi.org/10.1097/00024382-199902000-00018.

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3

Grippi, Michael A. „PULMONARY PATHOPHYSIOLOGY“. Shock 5, Nr. 4 (April 1996): 311. http://dx.doi.org/10.1097/00024382-199604000-00013.

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4

Chamarthy, Murthy R., Asha Kandathil und Sanjeeva P. Kalva. „Pulmonary vascular pathophysiology“. Cardiovascular Diagnosis and Therapy 8, Nr. 3 (Juni 2018): 208–13. http://dx.doi.org/10.21037/cdt.2018.01.08.

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5

Gao, Yuansheng, und J. Usha Raj. „Pathophysiology of Pulmonary Hypertension“. Colloquium Series on Integrated Systems Physiology: From Molecule to Function 9, Nr. 6 (22.11.2017): i—104. http://dx.doi.org/10.4199/c00158ed1v01y201710isp078.

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6

Angerio, Allan D., und Peter A. Kot. „Pathophysiology of pulmonary edema“. Critical Care Nursing Quarterly 17, Nr. 3 (November 1994): 21–26. http://dx.doi.org/10.1097/00002727-199411000-00004.

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7

Higenbottam, Tim. „Pathophysiology of Pulmonary Hypertension“. Chest 105, Nr. 2 (Februar 1994): 7S—12S. http://dx.doi.org/10.1378/chest.105.2_supplement.7s.

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8

Klayton, Ronald J. „PULMONARY PATHOPHYSIOLOGY — THE ESSENTIALS“. Military Medicine 158, Nr. 2 (01.02.1993): A9. http://dx.doi.org/10.1093/milmed/158.2.a9a.

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9

Shibuya, Kazutoshi, Chikako Hasegawa, Shigeharu Hamatani, Tsutomu Hatori, Tadashi Nagayama, Hiroko Nonaka, Tsunehiro Ando und Megumi Wakayama. „Pathophysiology of pulmonary aspergillosis“. Journal of Infection and Chemotherapy 10, Nr. 3 (2004): 138–45. http://dx.doi.org/10.1007/s10156-004-0315-5.

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10

Matthay, Michael A. „Pathophysiology of Pulmonary Edema“. Clinics in Chest Medicine 6, Nr. 3 (September 1985): 301–14. http://dx.doi.org/10.1016/s0272-5231(21)00366-x.

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11

Stroncek, David. „TRALI Pathophysiology.“ Blood 114, Nr. 22 (20.11.2009): SCI—48—SCI—48. http://dx.doi.org/10.1182/blood.v114.22.sci-48.sci-48.

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Abstract Abstract SCI-48 Transfusion related acute lung injury (TRALI) is clinically defined as the new onset of acute lung injury within 6 hours of a transfusion. In TRALI a transfusion activates neutrophils leading to pulmonary leukostasis, endothelial damage, capillary leak and pulmonary edema. A number of elements (bioactive lipids, sCD40L, and leukocyte antibodies) found in blood products can active neutrophils and are risk factors for TRALI. Bioactive lipids and sCD40L accumulate in both stored red cell and platelet components. Leukocyte antibodies are most often found in blood components collected from women alloimmunized during pregnancy. A number of animal and in vitro models have shown that neutrophils activated by leukocyte antibodies cause pulmonary leukostatsis, endothelial damage and capillary leak. Far more blood components contain these TRALI factors than cause TRALI suggesting that additional patient, clinical, or blood component factors are required for the development of TRALI. For example, neutrophil-specific antibodies cause reactions in, at most, 25% of transfusion recipients. Animal models and in vitro studies have found that blood component factors are more likely to induce lung injury if the neutrophils and/or pulmonary endothelial cells are primed or activated. Endothelial cells can be primed by endotoxin and neutrophils can be primed by bioactive lipids and sCD40L. The priming of neutrophils and /or endothelium results in the tight adhesion of neutrophils to endothelial cells and enhances endothelial cell injury Between neutrophil and HLA Class I and II antibodies, neutrophil antibodies are most potent at initiating TRALI and HLA Class I antibodies are least potent. HLA Class I antigens are expressed by platelets, lymphocytes, monocytes and soluble HLA Class I antigens are present in plasma. These sources of Class I antigens likely compete with neutrophils for transfused Class I antibodies and may render them less effective at initiating TRALI than neutrophil-specific or HLA Class II antibodies. Some evidence suggests that HLA Class I antibodies induce TRALI by binding to pulmonary endothelium and activating neutrophils through their Fc portion. Class II antibodies may initiate TRALI by binding to monocytes and stimulating cytokine release. In summary, TRALI is the result of patient and blood component factors which lead to neutrophil activation and endothelial cell damage and capillary leak. Most cases likely require the confluence of multiple factors to form a “perfect inflammatory storm” which leads to significant lung injury. Disclosures No relevant conflicts of interest to declare.
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12

Brudno, D. Spencer. „Pulmonary Vascular Physiology and Pathophysiology“. Journal of Asthma 27, Nr. 6 (Januar 1990): 413–14. http://dx.doi.org/10.3109/02770909009073361.

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13

Kulik, Thomas J. „Pathophysiology of acute pulmonary vasoconstriction“. Pediatric Critical Care Medicine 11 (März 2010): S10—S14. http://dx.doi.org/10.1097/pcc.0b013e3181c766c6.

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14

Dietz, Niki M. „Pathophysiology of Postpneumonectomy Pulmonary Edema“. Seminars in Cardiothoracic and Vascular Anesthesia 4, Nr. 1 (März 2000): 31–35. http://dx.doi.org/10.1177/108925320000400105.

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15

Jain, Suma, Hector Ventura und Ben deBoisblanc. „Pathophysiology of Pulmonary Arterial Hypertension“. Seminars in Cardiothoracic and Vascular Anesthesia 11, Nr. 2 (Juni 2007): 104–9. http://dx.doi.org/10.1177/1089253207301732.

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16

Plovsing, Ronni R., und Ronan M. G. Berg. „Pulmonary Pathophysiology in Another Galaxy“. Anesthesiology 120, Nr. 1 (01.01.2014): 230–32. http://dx.doi.org/10.1097/aln.0b013e31829c2dfb.

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17

Mason, Carol M., Warren R. Summer und Steve Nelson. „Pathophysiology of pulmonary defense mechanisms“. Journal of Critical Care 7, Nr. 1 (März 1992): 42–46. http://dx.doi.org/10.1016/0883-9441(92)90007-t.

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18

Genofre, Eduardo Henrique, Francisco S. Vargas, Lisete R. Teixeira, Marcelo Alexandre Costa Vaz und Evaldo Marchi. „Reexpansion pulmonary edema“. Jornal de Pneumologia 29, Nr. 2 (April 2003): 101–6. http://dx.doi.org/10.1590/s0102-35862003000200010.

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Reexpansion pulmonary edema (RPE) is a rare, but frequently lethal, clinical condition. The precise pathophysiologic abnormalities associated with this disorder are still unknown, though decreased pulmonary surfactant levels and a pro-inflammatory status are putative mechanisms. Early diagnosis is crucial, since prognosis depends on early recognition and prompt treatment. Considering the high mortality rates related to RPE, preventive measures are still the best available strategy for patient handling. This review provides a brief overview of the pathophysiology, diagnosis, treatment, and prevention of RPE, with practical recommendations for adequate intervention.
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19

Crausman, R. S., C. A. Jennings, R. M. Tuder, L. M. Ackerson, C. G. Irvin und T. E. King. „Pulmonary histiocytosis X: pulmonary function and exercise pathophysiology.“ American Journal of Respiratory and Critical Care Medicine 153, Nr. 1 (Januar 1996): 426–35. http://dx.doi.org/10.1164/ajrccm.153.1.8542154.

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20

West, John B. „Internet-based course on pulmonary pathophysiology“. Advances in Physiology Education 36, Nr. 1 (März 2012): 1–2. http://dx.doi.org/10.1152/advan.00125.2011.

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A course of seven video lectures on pulmonary pathophysiology has been placed on the internet. This is a companion to the course on respiratory physiology available at http://meded.ucsd.edu/ifp/jwest/ . That course dealt with normal respiratory physiology, and the new lectures are about the function of the diseased lung. The topics covered include pulmonary function tests, chronic obstructive pulmonary disease, asthma and localized airway obstruction, restrictive lung diseases, pulmonary vascular diseases, environmental or industrial lung diseases (with a short section on neoplastic and infectious diseases), and respiratory failure. Although it could be argued that PhD physiologists do not have a responsibility for teaching pathophysiology, collaborative teaching has become increasingly common in medical schools where, for example, a pulmonary block includes both normal respiratory physiology and some pulmonary pathophysiology. It is hoped that these lectures will be useful to physiologists in that setting.
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21

Jonathan, Steven, Triya Damayanti und Budhi Antariksa. „Pathophysiology of Emphysema“. Jurnal Respirologi Indonesia 39, Nr. 1 (02.01.2019): 60–69. http://dx.doi.org/10.36497/jri.v39i1.43.

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Pulmonary emphysema is part of pathological condition in chronic obstructive pulmonary disease (COPD) which is characterized by lung parenchymal destruction. Morphology classification of emphysema had been made according to histologic structure in pathology. There were some causes known to be the culprit of emphysema; one that caught most attention is protease-antiprotease activity from cigarette smoke exposure. Destructive effect of emphysema gives disturbance of lung function in expiration (obstruction). The primary mechanism is elastic recoil reduction which causes air trapping, lung volume increase, lung compliance increase and airways that is susceptible to collapse. Hyperinflation in emphysema causes some disadvantages which complicate inspiration and give a dyspnea sensation. Equal pressure point drop in emphysema happens because of elastic recoil reduction. This drop may cause early airway closure. (J Respir Indo 2019; 39(1): 60-9)
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22

Humbert, M. „Pulmonary arterial hypertension and chronic thromboembolic pulmonary hypertension: pathophysiology“. European Respiratory Review 19, Nr. 115 (28.02.2010): 59–63. http://dx.doi.org/10.1183/09059180.00007309.

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23

Lee, Sang-Do. „Pathophysiology of Chronic Obstructive Pulmonary Disease“. Journal of the Korean Medical Association 49, Nr. 4 (2006): 305. http://dx.doi.org/10.5124/jkma.2006.49.4.305.

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24

Milic-Emili, Joseph, Matteo Pecchiari und Edgardo D'Angelo. „Pathophysiology of Chronic Obstructive Pulmonary Disease“. Current Respiratory Medicine Reviews 4, Nr. 4 (01.11.2008): 250–57. http://dx.doi.org/10.2174/157339808786263842.

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25

Lan, Norris, Benjamin Massam, Sandeep Kulkarni und Chim Lang. „Pulmonary Arterial Hypertension: Pathophysiology and Treatment“. Diseases 6, Nr. 2 (16.05.2018): 38. http://dx.doi.org/10.3390/diseases6020038.

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26

Kim, Won Dong. „Pathophysiology of Chronic Obstructive Pulmonary Disease“. Tuberculosis and Respiratory Diseases 41, Nr. 5 (1994): 445. http://dx.doi.org/10.4046/trd.1994.41.5.445.

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27

Kim, Hyun Kuk, und Sang-Do Lee. „Pathophysiology of Chronic Obstructive Pulmonary Disease“. Tuberculosis and Respiratory Diseases 59, Nr. 1 (2005): 5. http://dx.doi.org/10.4046/trd.2005.59.1.5.

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28

Lynne-Davies, Patricia. „PULMONARY PATHOPHYSIOLOGY—THE ESSENTIALS, 3rd ed“. Chest 92, Nr. 4 (Oktober 1987): 24. http://dx.doi.org/10.1016/s0012-3692(16)31273-9.

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29

Haas, François, Randi Fain, John Salazar-Schicchi und Kenneth Axen. „Pathophysiology of Chronic Obstructive Pulmonary Disease“. Physical Medicine and Rehabilitation Clinics of North America 7, Nr. 2 (Mai 1996): 205–21. http://dx.doi.org/10.1016/s1047-9651(18)30393-0.

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30

Oliveira, Aline C., Elaine M. Richards und Mohan K. Raizada. „Pulmonary hypertension: Pathophysiology beyond the lung“. Pharmacological Research 151 (Januar 2020): 104518. http://dx.doi.org/10.1016/j.phrs.2019.104518.

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31

O'Donnell, Christopher P., Fernando Holguin und Anne E. Dixon. „Pulmonary physiology and pathophysiology in obesity“. Journal of Applied Physiology 108, Nr. 1 (Januar 2010): 197–98. http://dx.doi.org/10.1152/japplphysiol.01208.2009.

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32

NAGAI, SONOKO, und TAKATERU IZUMI. „Pulmonary Sarcoidosis: Population Differences and Pathophysiology“. Southern Medical Journal 88, Nr. 10 (Oktober 1995): 1001–10. http://dx.doi.org/10.1097/00007611-199510000-00002.

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33

Sysol, J. R., und R. F. Machado. „Classification and pathophysiology of pulmonary hypertension“. Continuing Cardiology Education 4, Nr. 1 (Juni 2018): 2–12. http://dx.doi.org/10.1002/cce2.71.

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34

Gonzalez, Norberto C. „Pulmonary Pathophysiology: The Essentials, 5th Edition“. Medicine & Science in Sports & Exercise 31, Nr. 1 (Januar 1999): 193–94. http://dx.doi.org/10.1097/00005768-199901000-00043.

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35

Thurlbeck, William M. „Pathophysiology of Chronic Obstructive Pulmonary Disease“. Clinics in Chest Medicine 11, Nr. 3 (September 1990): 389–403. http://dx.doi.org/10.1016/s0272-5231(21)00708-5.

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36

Simonneau, Gérald, Adam Torbicki, Peter Dorfmüller und Nick Kim. „The pathophysiology of chronic thromboembolic pulmonary hypertension“. European Respiratory Review 26, Nr. 143 (29.03.2017): 160112. http://dx.doi.org/10.1183/16000617.0112-2016.

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Chronic thromboembolic pulmonary hypertension (CTEPH) is a rare, progressive pulmonary vascular disease that is usually a consequence of prior acute pulmonary embolism. CTEPH usually begins with persistent obstruction of large and/or middle-sized pulmonary arteries by organised thrombi. Failure of thrombi to resolve may be related to abnormal fibrinolysis or underlying haematological or autoimmune disorders. It is now known that small-vessel abnormalities also contribute to haemodynamic compromise, functional impairment and disease progression in CTEPH. Small-vessel disease can occur in obstructed areas, possibly triggered by unresolved thrombotic material, and downstream from occlusions, possibly because of excessive collateral blood supply from high-pressure bronchial and systemic arteries. The molecular processes underlying small-vessel disease are not completely understood and further research is needed in this area. The degree of small-vessel disease has a substantial impact on the severity of CTEPH and postsurgical outcomes. Interventional and medical treatment of CTEPH should aim to restore normal flow distribution within the pulmonary vasculature, unload the right ventricle and prevent or treat small-vessel disease. It requires early, reliable identification of patients with CTEPH and use of optimal treatment modalities in expert centres.
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37

Shenoy, Vikram, James M. Anton, Charles D. Collard und Sloan C. Youngblood. „Pulmonary Thromboendarterectomy for Chronic Thromboembolic Pulmonary Hypertension“. Anesthesiology 120, Nr. 5 (01.05.2014): 1255–61. http://dx.doi.org/10.1097/aln.0000000000000228.

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Abstract Pulmonary thromboendarterectomy is the most effective therapy for chronic thromboembolic pulmonary hypertension. The pathophysiology, anesthetic management, and perioperative outcomes of patients with chronic thromboembolic pulmonary hypertension undergoing pulmonary thromboendarterectomy are reviewed.
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38

Widdicombe, J. G. „Nasal pathophysiology“. Respiratory Medicine 84 (November 1990): 3–10. http://dx.doi.org/10.1016/s0954-6111(08)80001-7.

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39

Kato, Hideyuki, Yaqin Yana Fu, Jiaquan Zhu, Lixing Wang, Shabana Aafaqi, Otto Rahkonen, Cameron Slorach et al. „Pulmonary vein stenosis and the pathophysiology of “upstream” pulmonary veins“. Journal of Thoracic and Cardiovascular Surgery 148, Nr. 1 (Juli 2014): 245–53. http://dx.doi.org/10.1016/j.jtcvs.2013.08.046.

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40

Chuchalin, A. G. „Pulmonary oedema: physiology of lung circulation, pathophysiology of pulmonary oedema“. PULMONOLOGIYA, Nr. 4 (28.08.2005): 9–18. http://dx.doi.org/10.18093/0869-0189-2005-0-4-9-18.

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41

Amariei, Diana E., Neal Dodia, Janaki Deepak, Stella E. Hines, Jeffrey R. Galvin, Sergei P. Atamas und Nevins W. Todd. „Combined Pulmonary Fibrosis and Emphysema: Pulmonary Function Testing and a Pathophysiology Perspective“. Medicina 55, Nr. 9 (10.09.2019): 580. http://dx.doi.org/10.3390/medicina55090580.

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Combined pulmonary fibrosis and emphysema (CPFE) has been increasingly recognized over the past 10–15 years as a clinical entity characterized by rather severe imaging and gas exchange abnormalities, but often only mild impairment in spirometric and lung volume indices. In this review, we explore the gas exchange and mechanical pathophysiologic abnormalities of pulmonary emphysema, pulmonary fibrosis, and combined emphysema and fibrosis with the goal of understanding how individual pathophysiologic observations in emphysema and fibrosis alone may impact clinical observations on pulmonary function testing (PFT) patterns in patients with CPFE. Lung elastance and lung compliance in patients with CPFE are likely intermediate between those of patients with emphysema and fibrosis alone, suggesting a counter-balancing effect of each individual process. The outcome of combined emphysema and fibrosis results in higher lung volumes overall on PFTs compared to patients with pulmonary fibrosis alone, and the forced expiratory volume in one second (FEV1)/forced vital capacity (FVC) ratio in CPFE patients is generally preserved despite the presence of emphysema on chest computed tomography (CT) imaging. Conversely, there appears to be an additive deleterious effect on gas exchange properties of the lungs, reflecting a loss of normally functioning alveolar capillary units and effective surface area available for gas exchange, and manifested by a uniformly observed severe reduction in the diffusing capacity for carbon monoxide (DLCO). Despite normal or only mildly impaired spirometric and lung volume indices, patients with CPFE are often severely functionally impaired with an overall rather poor prognosis. As chest CT imaging continues to be a frequent imaging modality in patients with cardiopulmonary disease, we expect that patients with a combination of pulmonary emphysema and pulmonary fibrosis will continue to be observed. Understanding the pathophysiology of this combined process and the abnormalities that manifest on PFT testing will likely be helpful to clinicians involved with the care of patients with CPFE.
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42

Tsuchiya, Nanae, Lindsay Griffin, Hidetake Yabuuchi, Satoshi Kawanami, Jintetsu Shinzato und Sadayuki Murayama. „Imaging findings of pulmonary edema: Part 1. Cardiogenic pulmonary edema and acute respiratory distress syndrome“. Acta Radiologica 61, Nr. 2 (21.06.2019): 184–94. http://dx.doi.org/10.1177/0284185119857433.

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Pulmonary edema has many causes; differentiating between these conditions is important. The purpose of this review article is to describe the pathophysiology of pulmonary edema, thereby explaining the imaging findings that differentiate between etiologies. Chest computed tomography provides details on the physiological response and the changes in the anatomical structures of pulmonary edema. An understanding of the pathophysiology underlying the imaging findings facilitates the correct identification of the cause of pulmonary edema.
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43

Nelson, Steve, Carol M. Mason, Jay Kolls und Warren R. Summer. „PATHOPHYSIOLOGY OF PNEUMONIA“. Clinics in Chest Medicine 16, Nr. 1 (März 1995): 1–12. http://dx.doi.org/10.1016/s0272-5231(21)00975-8.

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44

McCool, F. Dennis, und David E. Leith. „Pathophysiology of Cough“. Clinics in Chest Medicine 8, Nr. 2 (Juni 1987): 189–95. http://dx.doi.org/10.1016/s0272-5231(21)01014-5.

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45

Grissom, Colin K., und Mark R. Elstad. „The pathophysiology of high altitude pulmonary edema“. Wilderness & Environmental Medicine 10, Nr. 2 (Juni 1999): 88–92. http://dx.doi.org/10.1580/1080-6032(1999)010[0088:tpohap]2.3.co;2.

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46

Browne, George W. „Pathophysiology of pulmonary complications of acute pancreatitis“. World Journal of Gastroenterology 12, Nr. 44 (2006): 7087. http://dx.doi.org/10.3748/wjg.v12.i44.7087.

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47

Rubin, Lewis J. „Pathology and pathophysiology of primary pulmonary hypertension“. American Journal of Cardiology 75, Nr. 3 (Januar 1995): 51A—54A. http://dx.doi.org/10.1016/s0002-9149(99)80383-x.

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48

Qureshi, Amna Zafar, und Robert M. R. Tulloh. „Paediatric pulmonary hypertension: aetiology, pathophysiology and treatment“. Paediatrics and Child Health 27, Nr. 2 (Februar 2017): 50–57. http://dx.doi.org/10.1016/j.paed.2016.10.001.

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49

Bärtsch, P. „High-altitude pulmonary oedema: pathophysiology and treatment“. European Journal of Anaesthesiology 17, Supplement 20 (2000): 12. http://dx.doi.org/10.1097/00003643-200000003-00023.

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50

Davis, Pamela. „Pathophysiology of Pulmonary Disease in Cystic Fibrosis“. Seminars in Respiratory and Critical Care Medicine 6, Nr. 04 (April 1985): 261–70. http://dx.doi.org/10.1055/s-2007-1011505.

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