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Books on the topic 'Electrolytes Metabolism'

Author: Grafiati

Published: 4 June 2021

Last updated: 6 February 2022

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1

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

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2

Denise, Macklin, and Murphy-Ende Kathleen, eds. Fluids & electrolytes. 2nd ed. St. Louis: Elsevier Saunders, 2006.

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3

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

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4

A, Perazella Mark, ed. 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. 2nd ed. Oxford: Blackwell Scientific, 1987.

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6

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

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7

Jean, Weldy Norma, ed. Body fluids & electrolytes: A programmed presentation. 8th ed. St. Louis: Mosby, 2002.

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8

Fluids and electrolytes with clinical applications: A programmed approach. 4th ed. New York: Wiley, 1986.

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9

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

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10

J, Paulanka Betty, ed. Fluids and electrolytes with clinical applications: A programmed approach. 6th ed. Albany: Delmar, 2000.

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11

Kee, Joyce LeFever. Fluids and electrolytes with clinical applications: A programmed approach. 7th 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

S, Oh Man, ed. Water, electrolyte, and acid-base metabolism: Diagnosis and management. 2nd ed. Philadelphia: J.B. Lippincott, 1989.

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14

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

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15

B, Goldstein Marc, and Kamel Kamel S, eds. Fluid, electrolyte, and acid-base physiology: A problem-based approach. 4th ed. Philadelphia, PA: Saunders/Elsevier, 2009.

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16

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

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17

M, Brensilver Jeffrey, ed. A primer of water, electrolyte, and acid-base syndromes. 7th 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. Edited by Farthing M. J. G and Mahalanabis Dilip. Philadelphia: Lippincott Williams & Wilkins, 2003.

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21

1919-, Vanatta John C., and Fogelman Morris J. 1922-, eds. Moyer's fluid balance: A clinical manual. 4th ed. Chicago: Year Book Medical Publishers, 1988.

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22

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

Electrolytes. Trafalgar Square Publishing, 1994.

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27

Macklin, Denise, Ph D. Chernecky Cynthia, and 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

A, Young J., and Wong, P. Y. D., 1946-, eds. Epithelial secretion of water and electrolytes. Berlin: Springer-Verlag, 1990.

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30

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

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31

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

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32

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

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33

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

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34

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

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36

M, Szerlip Harold, and Goldfarb Stanley, eds. Workshops in fluid and electrolyte disorders. New York: Churchill Livingstone, 1993.

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37

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., and 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. Edited by 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), and 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, and 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. Edited by 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-, and 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-, and Narins Robert G, eds. Clinical disorders of fluid and electrolyte metabolism. 4th ed. New York: McGraw-Hill, 1987.

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49

(Editor), Thomas A. Pressley, and 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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