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Książki na temat „Acidosis”

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Autor: Grafiati

Data publikacji: 4 czerwca 2021

Data aktualizacji: 30 lipca 2024

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1

E. Wesson, Donald, red. Metabolic Acidosis. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3463-8.

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2

Muñoz, Ricardo, red. Renal Tubular Acidosis in Children. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-91940-5.

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3

Langbroek, Aart Jan Mattheüs. Metabolic acidosis and ventilatory response. Groningen: Drucker:] van Denderen, 1988.

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4

Arieff, Allen I., red. Hypoxia, Metabolic Acidosis, and the Circulation. New York, NY: Springer New York, 1992. http://dx.doi.org/10.1007/978-1-4614-7542-2.

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5

1938-, Arieff Allen I., i American Physiological Society (1887- ), red. Hypoxia, metabolic acidosis, and the circulation. New York: Published for the American Physiological Society by Oxford University Press, 1992.

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6

Parker, James N., i Philip M. Parker. The Official patient's sourcebook on renal tubular acidosis. San Diego, Calif: Icon Health Publications, 2002.

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7

Rai, Sharadindu. Protective effects of acidosis against stretch-induced lung injury. Ottawa: National Library of Canada, 2002.

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8

Chŏn, Yang-suk. Chongyang ŭi sansŏnghwa e ŭihan HIF-1[alpha] kwabarhyŏn kijŏn kyumyŏng kwa saeroun hangam chʻiryo tʻaget ŭi palgul =: Mechanism of HIF-1[alpha] overexpression in acidified tumor and novel target for anticancer therapy. [Seoul]: Pogŏn Pokchibu, 2007.

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9

John, Gennari F., red. Acid-base disorders and their treatment. Boca Raton: Taylor & Francis, 2005.

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10

Simonsohn, Barbara. Healing power of papaya: A holistic handbook on how to avoid acidosis, allergies, and other health disorders. Twin Lakes, WI: Lotus Light Publications, 2000.

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11

1920-, Seldin Donald W., i Giebisch Gerhard H, red. The Regulation of acid-base balance. New York: Raven Press, 1989.

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12

Cook, Michelle Schoffro. The Ultimate pH Solution. New York: HarperCollins, 2007.

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13

Cook, Michelle Schoffro. The ultimate pH solution: Balance your body chemistry to prevent disease and lose weight. New York: Collins, 2008.

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14

Krywawych, Steve. Metabolic Acidosis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0081.

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Hydrogen ion turnover in resting adults exceeds 500 mole/24 hours and maintenance of hydrogen ion balance is an essential requirement for normal cellular, organ and body function. A variety of mechanisms co-operate to ensure that the hydrogen concentration in plasma can be tightly controlled between 35 to 46 nano moles per litre and any deviation being rapidly compensated. Inherited metabolic diseases can to a variable degree impact to disturb this equilibrium. The underlying causes responsible for this outcome are disease dependent and may occur due to generation of overwhelming quantities of hydrogen per se, or at the level of renal reabsorption or generation of bicarbonate or due to tissue hypoxia resulting from either poor pulmonary or cardiac function.

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15

Staff, CIBA Foundation Symposium. Metabolic Acidosis. Wiley & Sons, Limited, John, 2008.

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16

Porter, Ruth, i Geralyn Lawrenson. Metabolic Acidosis. Wiley & Sons, Incorporated, John, 2009.

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17

The diagnosis of acidosis. [Toronto]: University Library, pub. by the Librarian, 1994.

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18

Yaqoob, Muhammad M. Acidosis in chronic kidney disease. Redaktor David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0148.

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Metabolic acidosis becomes increasingly common as chronic kidney disease progresses. It is associated with a number of complications, including bone disease, altered protein synthesis and degradation, skeletal muscle wasting, and lately progressive glomerular filtration rate loss. Experimental and clinical studies suggest a role for alkali therapy to lessen these complications. Recent controlled studies support this notion, and suggest that correction of metabolic acidosis in patients with chronic kidney disease slows the rate of decline of renal function and the development of end-stage renal disease, although more definitive evidence is needed on the long-term benefits of alkali therapy, type of alkali supplements, and the optimal level of serum bicarbonate.

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19

Acid Danger: Combating Acidosis Correctly. ReadHowYouWant.com, Limited, 2009.

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20

Acid Danger: Combating Acidosis Correctly. Basic Health Publications, Incorporated, 2004.

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21

Aver, Wolfgang R. Acid Danger: Combating Acidosis Correctly. Basic Health Publications, Incorporated, 2013.

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22

Acid Danger: Combating Acidosis Correctly. ReadHowYouWant.com, Limited, 2010.

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23

Walsh, Stephen B. Approach to the patient with renal tubular acidosis. Redaktor Robert Unwin. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0036.

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The renal tubular acidoses are a collection of syndromes characterized by defective urinary acidification. These syndromes have classically caused some confusion, and many opine that the widely used numerical system (type 1, 2) should be abandoned. We consider distal renal tubular acidosis and proximal renal tubular acidosis separately, and briefly cover hypoaldosteronism. Distal (Type 1) renal tubular acidosis is a syndrome of hypokalaemia, metabolic acidosis, kidney stones, nephrocalcinosis, and osteomalacia or rickets. It is caused by failure of the acid secreting α‎‎‎-intercalated cells in the distal nephron. Proximal (Type 2) renal tubular acidosis is a syndrome of metabolic acidosis that is almost always accompanied by the Fanconi syndrome of glycosuria, phosphaturia, uricosuria, aminoaciduria, and low-molecular-weight proteinuria. It is caused by a failure of bicarbonate reabsorption by the proximal tubular cells. Type 3 or mixed renal tubular acidosis, as originally described, has vanished (or was originally incompletely described). It is sometimes used to describe a mutation of carbonic anhydrase II, which causes both proximal and distal renal tubular acidosis, as well as cerebral calcification and osteopetrosis. Type 4 or hypoaldosteronism is a syndrome of hyperkalaemia and mild metabolic acidosis. It is due to a lack of aldosterone or resistance to its action.

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24

Wesson, Donald E. Metabolic Acidosis: A Guide to Clinical Assessment and Management. Springer, 2016.

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25

Wesson, Donald E. Metabolic Acidosis: A Guide to Clinical Assessment and Management. Springer London, Limited, 2016.

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26

Wesson, Donald E. Metabolic Acidosis: A Guide to Clinical Assessment and Management. Springer, 2018.

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27

The Acid Danger: Combating Acidosis Correctly. Basic Health Publications, 2004.

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28

Arieff, Allen I. Hypoxia, Metabolic Acidosis, and the Circulation. Springer, 2013.

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29

Monteiro, Carlos. Autonomic Dysfunction + Lactic Acidosis = Multiple Diseases. Independently Published, 2020.

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30

Gattinoni, Luciano, i Alfredo Lissoni. Pathophysiology and therapeutic strategy of respiratory acidosis. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0113.

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Out of 15–30 × 10–3 moles/day of protons derived from the hydration of CO2 only 40–60 × 10–9 moles/day remain unbounded in the plasma. If the CO2 production exceeds the excretion, the CO2 content in plasma and tissue rises (respiratory acidosis) until a new equilibrium is reached. In fact, doubling the PCO2 may compensate the halving of alveolar ventilation with unchanged excretion of the CO2 metabolically produced. Body reacts to respiratory acidosis increasing the secretion of chloride associated with ammonium. The process leads to an increase of bicarbonate in the plasma with an associated increase of pH. All the steps described may be altered in critically-ill patients due to hyper-metabolism, decreased excretion, decreased content of buffering proteins and impaired kidney response. Several options are available for therapy, from mechanical ventilation to artificial lung, up to lung transplant, depending on the severity of clinical conditions and their possible reversibility.

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31

Neligan, Patrick J., i Clifford S. Deutschman. Management of metabolic acidosis in the critically ill. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199600830.003.0256.

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Metabolic acidosis (MA) commonly complicates critical illness, usually manifesting as a fall in arterial pH (<7.4) accompanied by a concomitant fall in serum bicarbonate concentration. Acidosis caused by unmeasured anions (UMA), can be distinguished from Hyperchloraemic acidosis by demonstrating a widening of the anion gap (AG). AG should be corrected for albumin and lactate. The base deficit (BD) calculates degree of metabolic acidosis and represents the amount of strong cation required to restore the pH to 7.4. Neither the AG nor the BD specify the cause of acidosis, and are unhelpful in the setting of mixed disorders. The base deficit gap (BDG) is used to calculate the effect of free water, sodium, chloride and albumin on the BD. It is the difference between BDcalc and BDmeasured (on a blood gas) and represents UMA. The strong ion gap more robustly calculates the amount of UMA than AG or BDG, and may be more accurate at predicting outcomes in the emergency room. Lactic acidosis is due to hypovolaemia until otherwise proven. In the majority of cases aggressive fluid resuscitation is warranted. In the presence of normal tissue blood flow regional hypoperfusion, poisoning or exogenous catecholamines should be considered. Ketoacidosis is due to intracellular glucose deficiency, caused by hypoinsulinaemia or starvation. The former is treated with isotonic crystalloid and insulin. Renal acidosis is treated with renal replacement therapy or recovery of renal function.

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32

The spontaneous development of an acidosis condition in decerebrate cats. [Toronto]: University Library, pub. by the Librarian, 1994.

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33

Waldmann, Carl, Neil Soni i Andrew Rhodes. Metabolic disorders. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199229581.003.0024.

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Electrolyte disorders 410Hyponatraemia 414Hypernatraemia 416Categorizing metabolic acidoses 418Metabolic acidosis aetiology 420Metabolic alkalosis 422Glycaemic control in the critically ill 426Diabetic ketoacidosis 428Hyperosmolar diabetic emergencies 430Thyroid emergencies: thyroid crisis/thyrotoxic storm 432Thyroid emergencies: myxoedema coma 434Hypoadrenal crisis ...

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34

Halperin, Mitchell L., i Kamel S. Kamel. Approach to the patient with metabolic acidosis or alkalosis. Redaktor Robert Unwin. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0035_update_001.

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The pathophysiology, clinical approach, and management of the common causes of metabolic acidosis and alkalosis are discussed. In metabolic acidosis, a quantitative estimate of the extracellular volume (ECFV) is required to determine its content of bicarbonate in a patient with ECFV contraction. Buffering of H+ must occur by the bicarbonate buffer system in muscle to avoid binding to intracellular proteins, this requires low muscle capillary PCO2; acid gain type of metabolic acidosis is detected by the finding of new anions in blood and/or urine. The urine osmolal gap is the best indirect test to assess [NH4+] in urine. In metabolic alkalosis, Cl− depletion alkalosis is misleading. Deficits must be defined as HCl, KCl, and/or NaCl. A quantitative assessment of ECFV helps determine the contribution of individual deficits of Cl− salts. There is no tubular maximum for HCO3− reabsorption. Angiotensin II and the usual pH in proximal convoluted tubule cells, the two major stimuli for NaHCO3 reabsorption, must be removed/ changed for NaHCO3 to be excreted.

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35

Principles of Acidosis and Clinical Methods for Its Study. Creative Media Partners, LLC, 2022.

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36

Laforre. Acidosis: Index of New Information and Medical Research Bible. Abbe Pub Assn of Washington Dc, 1994.

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37

Laforee, Dr. Acidosis-Index of New Information and Medical Research Bible. Abbe Pub Assn of Washington Dc, 1994.

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38

Principles of Acidosis and Clinical Methods for Its Study. Creative Media Partners, LLC, 2022.

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39

Stratis, Danuta. Canker Sore Cures : the Link Between Acidosis and Canker Sores and the Healing Power of Amino Acids: Acidosis and Canker Sores. Independently Published, 2021.

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40

Neligan, Patrick J., i 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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41

Kirk, Esben. Acidosis: Clinical Aspects and Treatment with Isotonic Sodium Bicarbonate Solution. Elsevier Science & Technology Books, 2013.

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42

Wessig, H., L. Schmidt, H. Neumann, K. Lang i W. Ehrhardt. Säure-Basen-Gleichgewicht des Menschen: Grundlagen, Bestimmung und Interpretation in Diagnostik und Therapie. Steinkopff, Dietrich, 2013.

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43

Munoz, Ricardo. Renal Tubular Acidosis in Children: New Insights in Diagnosis and Treatment. Springer International Publishing AG, 2022.

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44

Publications, ICON Health. Acidosis - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References. ICON Health Publications, 2004.

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45

The onset of metabolic acidosis and the optimal speeds of walking and running. Ottawa: National Library of Canada, 1986.

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46

Publications, ICON Health. Lactic Acidosis - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References. ICON Health Publications, 2004.

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47

Publications, ICON Health. Metabolic Acidosis - A Medical Dictionary, Bibliography, and Annotated Research Guide to Internet References. ICON Health Publications, 2004.

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48

The Official Patient's Sourcebook on Renal Tubular Acidosis: A Directory for the Internet Age. Icon Health Publications, 2002.

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49

Janssen, Mirian C. H., i Shamima Rahman. Pyruvate Dehydrogenase Complex Deficiency. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199972135.003.0006.

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Pyruvate dehydrogenase complex (PDHc) deficiency usually first manifests at a young age and is rarely diagnosed in adulthood. The clinical picture varies from neonatal death with overwhelming lactic acidosis to a relatively benign course early in life. The three main presentations are congenital lactic acidosis, Leigh syndrome, and episodic ataxia. Treatment consists of a ketogenic diet and cofactor supplementation with thiamine. Successful therapy is rare.

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50

(Editor), F. John Gennari, Horacio J. Adrogue (Editor), John H. Galla (Editor) i Nicolaos Maddias (Editor), red. Acid-Base Disorders and Their Treatment. Informa Healthcare, 2005.

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