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Libros sobre el tema "Electrolytes Metabolism"

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Autor: Grafiati
Publicado: 4 de junio de 2021
Última modificación: 6 de febrero de 2022

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1

Chernecky, Cynthia C. Fluids & electrolytes. Philadelphia: W.B. Saunders, 2002.

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2

Chernecky, Cynthia C. Fluids & electrolytes. 2a ed. St. Louis: Elsevier Saunders, 2006.

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3

Chernecky, Cynthia C. Fluids & electrolytes. Philadelphia: Saunders, 2001.

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4

Reilly, Robert F. Acid-base, fluids and electrolytes. New York: McGraw-Hill, Medical Pub. Division, 2008.

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5

Willatts, Sheila M. Lecture notes on fluid and electrolyte balance. 2a ed. Oxford: Blackwell Scientific, 1987.

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6

Feld, Leonard G. Fluid and electrolytes in pediatrics: A comprehensive handbook. New York, NY: Humana Press, 2010.

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7

Speakman, Elizabeth. Body fluids & electrolytes: A programmed presentation. 8a ed. St. Louis: Mosby, 2002.

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8

Kee, Joyce LeFever. Fluids and electrolytes with clinical applications: A programmed approach. 4a ed. New York: Wiley, 1986.

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9

Kee, Joyce LeFever. Fluids and electrolytes with clinical applications: A programmed approach. 5a ed. Albany, NY: Delmar Publishers, 1994.

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10

Kee, Joyce LeFever. Fluids and electrolytes with clinical applications: A programmed approach. 6a ed. Albany: Delmar, 2000.

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11

Kee, Joyce LeFever. Fluids and electrolytes with clinical applications: A programmed approach. 7a ed. Clifton Park, NY: Delmar, 2004.

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12

Eccles, Ronald. Electrolytes, body fluids and acid base balance. London: E. Arnold, a division of Hodder & Stoughton, 1993.

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13

Carroll, Hugh J. Water, electrolyte, and acid-base metabolism: Diagnosis and management. 2a ed. Philadelphia: J.B. Lippincott, 1989.

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14

Halperin, M. L. Fluid, electrolyte, and acid-base physiology: A problem-based approach. 2a ed. Philadelphia: W.B. Saunders, 1994.

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15

Halperin, M. L. Fluid, electrolyte, and acid-base physiology: A problem-based approach. 4a ed. Philadelphia, PA: Saunders/Elsevier, 2009.

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16

Halperin, M. L. Fluid, electrolyte, and acid-base physiology: A problem-based approach. 3a ed. Philadelphia: W.B. Saunders, 1999.

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17

Goldberger, Emanuel. A primer of water, electrolyte, and acid-base syndromes. 7a ed. Philadelphia: Lea & Febiger, 1986.

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18

McDougal, W. Scott. Fluid, electrolyte, and metabolic problems common to urologic practice. Bellaire, Tex. (6750 W. Loop South, Suite 900, Bellaire 77401): American Urological Association, Office of Education, 1987.

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19

Mottaghitalab, Majib. No n-electrolyte metabolism and absorption in the proximal gastrointestinal tract. Manchester: University of Manchester, 1996.

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20

Nestlé Nutrition Workshop (51st 2002 New Delhi, India). The control of food and fluid intake in health and disease. Editado por Farthing M. J. G y Mahalanabis Dilip. Philadelphia: Lippincott Williams & Wilkins, 2003.

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21

Moyer, Carl A. Moyer's fluid balance: A clinical manual. 4a ed. Chicago: Year Book Medical Publishers, 1988.

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22

Grossman, Sebastian Peter. Thirst and sodium appetite: Physiological basis. San Diego: Academic Press, 1990.

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23

Kravik, Stein E. Cardiovascular, renal, electrolyte, and hormonal changes in man during gravitational stress, weightlessness, and simulated weightlessness: Lower body positive pressure applied by the antigravity suit. Moffett Field, Calif: National Aeronautics and Space Administration, Ames Research Center, 1989.

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24

Adrogué, Horacio J. Salt & water. Boston: Blackwell Scientific Publications, 1994.

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25

Eknoyan, G. Electrolytes & Acute Renal Failure (Mineral and Electrolyte Metabolism,). S. Karger AG (Switzerland), 1991.

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26

Eccles y Ronald Eccles. Electrolytes. Trafalgar Square Publishing, 1994.

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27

Macklin, Denise, Ph D. Chernecky Cynthia y Ph D. Murphy-Ende Kathleen. Real-World Nursing Survival Guide Fluids & Electrolytes. W.B. Saunders Company, 2001.

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28

Kee, Joyce LeFever. Fluids and Electrolytes with Clinical Applications. Delmar, 1989.

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29

Epithelial secretion of water and electrolytes. Berlin: Springer-Verlag, 1990.

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30

Macklin, Denise, Kathleen Murphy-Ende y Cynthia C. Chernecky. Saunders Nursing Survival Guide: Fluids and Electrolytes (Saunders Nursing Survival Guide). 2a ed. Saunders, 2005.

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31

Kee, Joyce LeFever y Betty J. Paulanka. Fluids and Electrolytes with Clinical Applications: A Programmed Approach. 6a ed. Delmar Thomson Learning, 1999.

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32

Speakman, Elizabeth y Norma J. Weldy. Body Fluids and Electrolytes: A Programmed Presentation. 8a ed. Mosby, 2001.

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33

Kee, Joyce LeFever, Betty J. Paulanka y Larry Purnell. Fluid and Electrolytes with Clinical Applications: A Programmed Approach 7e. 7a ed. Cengage Delmar Learning, 2003.

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34

Reilly, Robert F. y Mark Perazella. Lange Instant Access: Acid-Base, Fluids, and Electrolytes (Lange Instant Access). McGraw-Hill Professional, 2007.

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35

Reilly, Robert F. y Mark Perazella. Lange Instant Access: Acid-Base, Fluids, and Electrolytes (Lange Instant Access). McGraw-Hill Professional, 2007.

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36

Workshops in fluid and electrolyte disorders. New York: Churchill Livingstone, 1993.

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37

VanLancker, J. L. Molecular and Cellular Mechanisms in Disease : 1: Bioenergetics · Cell Specificity · Inborn Errors of Metabolism · Malnutrition · Calcium and ... · Hormones Body Fluids and Electrolytes. Springer, 2011.

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38

Neligan, Patrick J. y Clifford S. Deutschman. Pathophysiology and causes of metabolic acidosis in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0255.

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Critical illness is typically characterized by changes in the balance of water and electrolytes in the extracellular space, resulting in the accumulation of anionic compounds that manifests as metabolic acidosis. Metabolic acidosis manifests with tachypnoea, tachycardia, vasodilatation, headache and a variety of other non-specific symptoms and signs. It is caused by a reduction in the strong ion difference (SID) or an increase in weak acid concentration (albumin or phosphate). Increased SID results from hyperchloraemia, haemodilution or accumulation of metabolic by-products. A reduction in SID results in a corresponding reduction is serum bicarbonate. There is a corresponding increase in alveolar ventilation and reduced PaCO2. Lactic acidosis results from increased lactate production or reduced clearance. Ketoacidosis is associated with reduced intracellular glucose availability for metabolism, and is associated with insulin deficiency and starvation. Hyperchloraemic acidosis is associated with excessive administration of isotonic saline solution, renal tubular acidosis and ureteric re-implantation. Renal acidosis is associated with hyperchloraemia, hyperphosphataemia, and the accumulation of medley nitrogenous waste products.
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39

Ho, Kwok M. Kidney and acid–base physiology in anaesthetic practice. Editado por Jonathan G. Hardman. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199642045.003.0005.

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Anatomically the kidney consists of the cortex, medulla, and renal pelvis. The kidneys have approximately 2 million nephrons and receive 20% of the resting cardiac output making the kidneys the richest blood flow per gram of tissue in the body. A high blood and plasma flow to the kidneys is essential for the generation of a large amount of glomerular filtrate, up to 125 ml min−1, to regulate the fluid and electrolyte balance of the body. The kidneys also have many other important physiological functions, including excretion of metabolic wastes or toxins, regulation of blood volume and pressure, and also production and metabolism of many hormones. Although plasma creatinine concentration has been frequently used to estimate glomerular filtration rate by the Modification of Diet in Renal Disease (MDRD) equation in stable chronic kidney diseases, the MDRD equation has limitations and does not reflect glomerular filtration rate accurately in healthy individuals or patients with acute kidney injury. An optimal acid–base environment is essential for many body functions, including haemoglobin–oxygen dissociation, transcellular shift of electrolytes, membrane excitability, function of many enzymes, and energy production. Based on the concepts of electrochemical neutrality, law of conservation of mass, and law of mass action, according to Stewart’s approach, hydrogen ion concentration is determined by three independent variables: (1) carbon dioxide tension, (2) total concentrations of weak acids such as albumin and phosphate, and (3) strong ion difference, also known as SID. It is important to understand that the main advantage of Stewart over the bicarbonate-centred approach is in the interpretation of metabolic acidosis.
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40

Nutrition & Metabolism in Renal Disease (Mineral and Electrolyte Metabolism). S. Karger AG (Switzerland), 1992.

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41

(Editor), Shaul G. Massry, A. Heidland (Editor), J. D. Kopple (Editor), J. Bergstrok (Editor) y A. Alvestrand (Editor), eds. Nutrition & Metabolism in Renal Disease: International Society of Renal Nutrition & Metabolism (Journal: Mineral & Electrolyte Metabolis Series, 1-3). S Karger Pub, 1995.

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42

Quamme, Gary A. Magnesium Homeostasis (Mineral and Electrolyte Metabolism). S. Karger AG (Switzerland), 1993.

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43

Peri, Alessandro, Chris J. Thompson y Joseph G. Verbalis, eds. Disorders of Fluid and Electrolyte Metabolism. S. Karger AG, 2019. http://dx.doi.org/10.1159/isbn.978-3-318-06383-7.

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44

Maroni, Bradley J. Protein Metabolism in Renal Diseases (Mineral & Electrolyte Metabolism Ser. 1). S Karger Pub, 1997.

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45

Saxena, Anjali Bhatt. Peritoneal dialysis. Editado por Jonathan Himmelfarb. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0265.

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Dialysis adequacy is a term used to describe how well any dialysis therapy effectively mitigates some of the uraemic complications of end-stage renal disease. In the simplest terms, dialysis adequacy measures the dose of dialysis and judges it to be sufficient (adequate) or insufficient (inadequate). In peritoneal dialysis, adequacy refers to the ability of dialysis to perform any or all of myriad tasks including (a) removing metabolic waste products, (b) maintaining proper fluid balance and blood pressure control, (c) removing excess electrolytes, (d) correcting acid–base imbalances, (e) maintaining healthy bone mineral metabolism, and (f) promoting the maintenance of a proper nutritional status. In practice, peritoneal dialysis adequacy is most often measured mono-dimensionally, in terms of small solute (i.e. urea) clearances; however, it is most useful to incorporate a wider view of dialysis adequacy when caring for patients with end-stage renal disease.
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46

Salt and Hypertension: Dietary Minerals, Volume Homeostasis and Cardiovascular Regulation. Springer, 1989.

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47

1953-, Rettig R., Ganten D. 1941- y Luft F. C. 1942-, eds. Salt and hypertension: Dietary minerals, volume homeostatis, and cardiovascular regulation. Berlin: Springer-Verlag, 1989.

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48

1924-, Maxwell Morton H., Kleeman Charles R. 1923- y Narins Robert G, eds. Clinical disorders of fluid and electrolyte metabolism. 4a ed. New York: McGraw-Hill, 1987.

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49

(Editor), Thomas A. Pressley y Sandra Sabatini (Editor), eds. The Atpases (Mineral & Electrolyte Metabolism, 5-6). S Karger Pub, 1996.

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50

G, Dluhy Robert, ed. Clinical disorders of fluid and electrolyte metabolism. Philadelphia: Saunders, 1995.

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