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Journal articles on the topic 'Pathophysiology'

Author: Grafiati

Published: 4 June 2021

Last updated: 30 July 2024

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1

Evans, Roger. "Campbell’s Pathophysiology NotesCampbell’s Pathophysiology Notes." Nursing Standard 21, no. 30 (April 4, 2007): 31. http://dx.doi.org/10.7748/ns2007.04.21.30.31.b600.

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2

Huether, Sue E., and Kathryn L. McCance. "Pathophysiology." Dimensions of Critical Care Nursing 13, no. 6 (November 1994): 315. http://dx.doi.org/10.1097/00003465-199411000-00010.

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3

Werkö, Lars. "PATHOPHYSIOLOGY." Acta Medica Scandinavica 210, S652 (April 24, 2009): 9–11. http://dx.doi.org/10.1111/j.0954-6820.1981.tb06781.x.

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4

Zreik, Tony G., and David L. Olive. "PATHOPHYSIOLOGY." Obstetrics and Gynecology Clinics of North America 24, no. 2 (June 1997): 259–68. http://dx.doi.org/10.1016/s0889-8545(05)70303-x.

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5

Rothwell, J. "Pathophysiology." Electroencephalography and Clinical Neurophysiology 103, no. 1 (July 1997): 48. http://dx.doi.org/10.1016/s0013-4694(97)88121-0.

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6

Komenaka, Ian. "Pathophysiology." Current Surgery 58, no. 2 (March 2001): 186–87. http://dx.doi.org/10.1016/s0149-7944(00)00433-5.

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7

Woolf, N. "Pathophysiology." Journal of Clinical Pathology 39, no. 8 (August 1, 1986): 931. http://dx.doi.org/10.1136/jcp.39.8.931-a.

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8

Kersey, Robert D. "Pathophysiology." Athletic Therapy Today 10, no. 2 (March 2005): 60–61. http://dx.doi.org/10.1123/att.10.2.60.

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9

Dudley, Sharon L. "Pathophysiology." Gastroenterology Nursing 15, no. 5 (April 1993): 212. http://dx.doi.org/10.1097/00001610-199304000-00010.

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10

Shepeleva, A. D., D. F. Shamardanov, and E. V. Ponomarenko. "PATHOPHYSIOLOGY OF MULTIPLE SCLEROSIS." European Journal of Natural History, no. 4 2022 (2022): 12–16. http://dx.doi.org/10.17513/ejnh.34281.

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11

Holle, Dagny, Steffen Naegel, and Mark Obermann. "Pathophysiology of hypnic headache." Cephalalgia 34, no. 10 (May 29, 2014): 806–12. http://dx.doi.org/10.1177/0333102414535996.

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Background Hypnic headache (HH) is a rare primary headache disorder that is characterized by strictly sleep related headache attacks. Purpose The underlying pathophysiology of HH is mainly enigmatic but some clinical characteristics such as circadian rhythmicity and caffeine responsiveness may point toward possible underlying mechanisms. Method Current studies that deal with the pathophysiology of HH are summarized. Data on cerebral imaging, sleep, electrophysiology studies, effectiveness of drugs, and symptomatic headache types are discussed to illuminate underlying pathophysiologic mechanisms. Conclusion HH can be clearly differentiated by its clinical presentation as well as imaging and electrophysiological study results from other primary headaches such as migraine or cluster headache. The underlying pathophysiology is still enigmatic but a hypothalamic involvement seems to be likely.

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12

McGurk, Simon. "Understanding Pathophysiology – Fifth editionUnderstanding Pathophysiology – Fifth edition." Nursing Standard 26, no. 49 (August 8, 2012): 30. http://dx.doi.org/10.7748/ns2012.08.26.49.30.b1393.

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13

khan, Nida Tabassum, and Ali Ijaz. "Migraine-Current Understanding and Pathophysiology." Journal of Clinical and Laboratory Research 5, no. 4 (March 31, 2022): 01–04. http://dx.doi.org/10.31579/2768-0487/079.

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A migraine is a headache episode ordinarily happens in stages and can keep going for a considerable length of time. Serious cases can influence an individual's everyday existence, including their capacity to work or study. Headache can influence individuals in various ways, and the triggers, seriousness, manifestations, and recurrence can change. Certain individuals have more than one episode every week, while others have them just incidentally. The reasons for migraine aren't actually clear, however hereditary qualities and climate really do assume a part. Migraine frequently runs in families, so there's probable an inherited connection.

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14

Kimura, Kazumi. "I. Pathophysiology." Nihon Naika Gakkai Zasshi 98, no. 6 (2009): 1224–30. http://dx.doi.org/10.2169/naika.98.1224.

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15

Bozoghlanian, Mari, and Sridhar Vasudevan. "Migraine pathophysiology." Pain Management 1, no. 4 (July 2011): 337–52. http://dx.doi.org/10.2217/pmt.11.34.

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16

Silberberg, A. "II. Pathophysiology." Clinical Hemorheology and Microcirculation 2, no. 5-6 (December 9, 2016): 509. http://dx.doi.org/10.3233/ch-1982-25-609.

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17

Franjić, Siniša. "Renal Pathophysiology." International Journal of Research Studies in Medical and Health Sciences 5, no. 10 (2020): 15–20. http://dx.doi.org/10.22259/ijrsmhs.0510005.

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18

Vincent, Tonia L., Tamara Alliston, Mohit Kapoor, Richard F. Loeser, Linda Troeberg, and Christopher B. Little. "Osteoarthritis Pathophysiology." Clinics in Geriatric Medicine 38, no. 2 (May 2022): 193–219. http://dx.doi.org/10.1016/j.cger.2021.11.015.

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19

Yamamoto, Toshiyuki. "Scleroderma – Pathophysiology." European Journal of Dermatology 19, no. 1 (January 2009): 014–24. http://dx.doi.org/10.1684/ejd.2008.0570.

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20

Cherniack, Neil S. "Pulmonary Pathophysiology." Annals of Internal Medicine 131, no. 5 (September 7, 1999): 399. http://dx.doi.org/10.7326/0003-4819-131-5-199909070-00022.

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21

Fan, Chieh-Min. "Venous Pathophysiology." Seminars in Interventional Radiology 22, no. 03 (September 2005): 157–61. http://dx.doi.org/10.1055/s-2005-921949.

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22

HUBBARD, ROGER W. "Heatstroke pathophysiology." Medicine & Science in Sports & Exercise 22, no. 1 (February 1990): 19???28. http://dx.doi.org/10.1249/00005768-199002000-00005.

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23

Grippi, Michael A. "PULMONARY PATHOPHYSIOLOGY." Shock 5, no. 4 (April 1996): 311. http://dx.doi.org/10.1097/00024382-199604000-00013.

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24

Sandberg, R., and M. Grady. "Pathophysiology course." Academic Medicine 60, no. 10 (October 1985): 816–7. http://dx.doi.org/10.1097/00001888-198510000-00016.

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25

AUGUSTIN, A. "General Pathophysiology." Acta Ophthalmologica 89, s248 (September 2011): 0. http://dx.doi.org/10.1111/j.1755-3768.2011.4313.x.

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26

Van Horn, Elizabeth R., Yolanda M. Hyde, Anita S. Tesh, and Donald D. Kautz. "Teaching Pathophysiology." Nurse Educator 39, no. 1 (2014): 34–37. http://dx.doi.org/10.1097/01.nne.0000437364.19090.be.

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27

Tomberg, Claude. "Alcohol Pathophysiology." Journal of Psychophysiology 24, no. 4 (January 2010): 215–30. http://dx.doi.org/10.1027/0269-8803/a000035.

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There is no specialized alcohol addiction area in the brain; rather, alcohol acts on a wide range of excitatory and inhibitory nervous networks to modulate neurotransmitters actions by binding with and altering the function of specific proteins. With no hemato-encephalic barrier for alcohol, its actions are strongly related to the amount of intake. Heavy alcohol intake is associated with both structural and functional changes in the central nervous system with long-term neuronal adaptive changes contributing to the phenomena of tolerance and withdrawal. The effects of alcohol on the function of neuronal networks are heterogeneous. Because ethanol affects neural activity in some brain sites but is without effect in others, its actions are analyzed in terms of integrated connectivities in the functional circuitry of neuronal networks, which are of particular interest because of the cognitive interactions discussed in the manuscripts contributing to this review. Recent molecular data are reviewed as a support for the other contributions dealing with cognitive disturbances related to alcohol acute and addicted consumption.

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28

Hallett, Mark. "Tremor: Pathophysiology." Parkinsonism & Related Disorders 20 (January 2014): S118—S122. http://dx.doi.org/10.1016/s1353-8020(13)70029-4.

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29

Goadsby, Peter J. "Migraine Pathophysiology." Headache: The Journal of Head and Face Pain 45, s1 (April 2005): S14—S24. http://dx.doi.org/10.1111/j.1526-4610.2005.4501003.x.

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30

Germon, Karin. "Understanding Pathophysiology." Journal of Neuroscience Nursing 29, no. 1 (February 1997): 58–59. http://dx.doi.org/10.1097/01376517-199702000-00013.

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31

Qubty, William, and Irene Patniyot. "Migraine Pathophysiology." Pediatric Neurology 107 (June 2020): 1–6. http://dx.doi.org/10.1016/j.pediatrneurol.2019.12.014.

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32

Kryzhanovsky, G. N. "Modern pathophysiology." Pathophysiology 1, no. 1 (May 1994): 1–3. http://dx.doi.org/10.1016/s0928-4680(05)80001-x.

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33

Brouwer, Patrick A., Waleed Brinjikji, and Simon F. De Meyer. "Clot Pathophysiology." Neuroimaging Clinics of North America 28, no. 4 (November 2018): 611–23. http://dx.doi.org/10.1016/j.nic.2018.06.005.

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34

Cimpello, Lynn Babcock, David L. Goldman, and Hnin Khine. "Fever pathophysiology." Clinical Pediatric Emergency Medicine 1, no. 2 (March 2000): 84–93. http://dx.doi.org/10.1016/s1522-8401(00)90012-0.

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35

Eisele, Charlie. "Pathophysiology: Paramedic." JEMS: Journal of Emergency Medical Services 33, no. 7 (July 2008): 125. http://dx.doi.org/10.1016/s0197-2510(08)70270-5.

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36

Gewertz, Bruce L. "Surgical pathophysiology." Journal of Vascular Surgery 15, no. 5 (May 1992): 942. http://dx.doi.org/10.1016/0741-5214(92)90769-5.

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37

Mary, David A. S. G. "Cardiovascular Pathophysiology." International Journal of Cardiology 16, no. 3 (September 1987): 327–28. http://dx.doi.org/10.1016/0167-5273(87)90165-3.

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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

Gonzalez, Norberto C. "PULMONARY PATHOPHYSIOLOGY." Shock 11, no. 2 (February 1999): 152. http://dx.doi.org/10.1097/00024382-199902000-00018.

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40

Olsen, E. "Cardiovascular Pathophysiology." Journal of Clinical Pathology 41, no. 7 (July 1, 1988): 816. http://dx.doi.org/10.1136/jcp.41.7.816-a.

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41

Winfield, D. "Blood: Pathophysiology." Journal of Clinical Pathology 44, no. 11 (November 1, 1991): 968. http://dx.doi.org/10.1136/jcp.44.11.968-a.

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42

Low, Walter C. "Cerebral Pathophysiology." Neurosurgery 32, no. 5 (May 1, 1993): 874–75. http://dx.doi.org/10.1227/00006123-199305000-00033.

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43

Mulkey, Malissa A., Sonya R. Hardin, DaiWai M. Olson, and Cindy L. Munro. "Pathophysiology Review." Clinical Nurse Specialist 32, no. 4 (2018): 195–211. http://dx.doi.org/10.1097/nur.0000000000000384.

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44

Stroncek, David. "TRALI Pathophysiology." Blood 114, no. 22 (November 20, 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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45

&NA;. "Pathophysiology review." Nursing 40, no. 4 (April 2010): 46–47. http://dx.doi.org/10.1097/01.nurse.0000369866.13552.7e.

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46

Low, Walter C. "Cerebral Pathophysiology." Neurosurgery 32, no. 5 (May 1993): 874???875. http://dx.doi.org/10.1097/00006123-199305000-00033.

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47

Ellis, H. "Surgical Pathophysiology." Postgraduate Medical Journal 68, no. 800 (June 1, 1992): 491. http://dx.doi.org/10.1136/pgmj.68.800.491.

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48

Remuzzi, Giuseppe. "Renal pathophysiology." Current Opinion in Nephrology and Hypertension 2, no. 4 (July 1993): 597–601. http://dx.doi.org/10.1097/00041552-199307000-00010.

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49

&NA;, &NA;. "Renal pathophysiology." Current Opinion in Nephrology and Hypertension 2, no. 4 (July 1993): 683–86. http://dx.doi.org/10.1097/00041552-199307000-00020.

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50

Remuzzi, Giuseppe. "Renal pathophysiology." Current Opinion in Nephrology and Hypertension 3, no. 4 (July 1994): 431–35. http://dx.doi.org/10.1097/00041552-199407000-00009.

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