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Lactic acidosis

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720:. As more lactate accumulates and rumen pH drops, the ruminal concentration of undissociated lactic acid increases. Undissociated lactic acid can cross the rumen wall to the blood, where it dissociates, lowering blood pH. Both L and D isomers of lactic acid are produced in the rumen; these isomers are metabolized by different metabolic pathways, and activity of the principal enzyme involved in metabolism of the D isomer declines greatly with lower pH, tending to result in an increased ratio of D:L isomers as acidosis progresses. 69: 43: 648:) for intense movements, can be particularly susceptible to lactic acidosis. In particular, during the capture of large crocodiles, the animals' use of their glycolytic muscles often alters the blood's pH to a point where they are unable to respond to stimuli or move. Cases are recorded in which particularly large crocodiles which put up extreme resistance to capture later died of the resulting pH imbalance. 724:
or monensin in feed can reduce risk of lactic acidosis in ruminants, inhibiting most of the lactate-producing bacterial species without inhibiting the major lactate fermenters. Also, using a higher feeding frequency to provide the daily grain ration can allow higher grain intake without reducing the pH of the rumen fluid.
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Measures for preventing lactic acidosis in ruminants include avoidance of excessive amounts of grain in the diet, and gradual introduction of grain over a period of several days, to develop a rumen population capable of safely dealing with a relatively high grain intake. Administration of lasalocid
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In domesticated ruminants, lactic acidosis may occur as a consequence of ingesting large amounts of grain, especially when the rumen population is poorly adapted to deal with grain. Activity of various rumen organisms results in accumulation of various volatile fatty acids (normally, mostly acetic,
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Lactic Acidosis refers to the process leading to the production of lactate by anaerobic metabolism. It increases hydrogen ion concentration tending to the state of acidemia or low pH. The result can be detected with high levels of lactate and low levels of bicarbonate. This is usually considered the
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in ten enzymatic steps. A significant proportion of pyruvate is converted into lactate (the blood lactate-to-pyruvate ratio is normally 10:1). The human metabolism produces about 20 mmol/kg of lactic acid every 24 hours. This happens predominantly in tissues (especially muscle) that have high
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In "type A" lactic acidosis, the production of lactate is attributable to insufficient oxygen for aerobic metabolism. If there is no oxygen available for the parts of the glucose metabolism that require oxygen (citric acid cycle and oxidative phosphorylation), excess pyruvate will be converted in
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Treatment of lactic acidosis in ruminants may involve intravenous administration of dilute sodium bicarbonate, oral administration of magnesium hydroxide, and/or repeated removal of rumen fluids and replacement with water (followed by reinoculation with rumen organisms, if necessary).
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Because of the high solute concentration of the rumen fluid under such conditions, considerable water is translocated from the blood to the rumen along the osmotic potential gradient, resulting in dehydration which cannot be relieved by drinking, and which can ultimately lead to
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Lactic acidosis is classically defined as an elevated lactate together with pH < 7.35 and bicarbonate below 20 mmol/L, but this is not required as lactic acidosis may exist together with other acid-base abnormalities that may affect these two parameters.
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Elevations in lactate are either a consequence of increased production or of decreased metabolism. With regards to metabolism, this predominantly takes place in the liver (70%), which explains that lactate levels may be elevated in the setting of liver disease.
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McKenzie, Robin; Fried, Michael W.; Sallie, Richard; Conjeevaram, Hari; Di Bisceglie, Adrian M.; Park, Yoon; Savarese, Barbara; Kleiner, David; Tsokos, Maria; Luciano, Carlos; Pruett, Timothy; Stotka, Jennifer L.; Straus, Stephen E.; Hoofnagle, Jay H. (1995).
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excess lactate. In "type B" lactic acidosis the lactate accumulates because there is a mismatch between glycolysis activity and the remainder of glucose metabolism. Examples are situations where the
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and some other organisms. With high grain consumption, the concentration of dissociated organic acids can become quite high, resulting in rumen pH dropping below 6. Within this lower pH range,
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to provide the majority of their energy needs. Adaptations in particular in the turtle's blood composition and shell allow it to tolerate high levels of lactic acid accumulation. In the
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Baertling, F; Rodenburg, R. J; Schaper, J; Smeitink, J. A; Koopman, W. J. H; Mayatepek, E; Morava, E; Distelmaier, F (2013). "A guide to diagnosis and treatment of Leigh syndrome".
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conditions where fermentation is dominant, calcium levels in the blood plasma increase. This calcium serves as a buffer, reacting with the excess lactate to form the precipitate
508:). There is controversy as to whether elevated lactate in acute illness can be attributed to tissue hypoxia; there is limited empirical support for this theoretical notion. 281:(MALA) increases in certain situations where both the plasma levels of metformin are increased and lactate clearance is impaired. The older related and now withdrawn drug 686:
propionic, and butyric acids), which are partially dissociated. Although some lactate is normally produced in the rumen, it is normally metabolized by such organisms as
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Santini, A; Ronchi, D; Garbellini, M; Piga, D; Protti, A (July 2017). "Linezolid-induced lactic acidosis: the thin line between bacterial and mitochondrial ribosomes".
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into lactate. The lactate is carried by the bloodstream to other tissues where it is converted back to pyruvate by the "B" isoform of LDH (LDHB). Firstly there is
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Mild and transient elevations in lactate have limited impact on mortality, whereas sustained and severe lactate elevations are associated with a high mortality.
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Kaufmann W (1976). "Influence of the composition of the ration and the feeding frequency on ph-regulation in the rumen and on feed in-take in ruminants".
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is also available as an alternative as they are effectively interchangeable. Normally resulting lactate concentrations are in the range indicated below:
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of lactic acid is low, about 3.9, versus, for example, 4.8 for acetic acid; this contributes to the considerable drop in rumen pH which can occur.
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Certain turtle species have been found to be capable of tolerating high levels of lactic acid without experiencing the effects of lactic acidosis.
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Kajbaf, F; Lalau, JD (November 2014). "Mortality rate in so-called "metformin-associated lactic acidosis": a review of the data since the 1960s".
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The mortality of lactic acidosis in people taking metformin was previously reported to be 50%, but in more recent reports this was closer to 25%.
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in the liver (as well as the kidney and some other tissues), where lactate is converted into pyruvate and then into glucose; this is known as the
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samples), and once confirmed, generally prompts an investigation to establish the underlying cause to treat the acidosis. In some situations,
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Nagaraja, TG; Avery, TB; Bartley, EE; Galitzer, SJ; Dayton, AD (1981). "Prevention of lactic acidosis in cattle by lasalocid or monensin".
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Lactic acidosis is commonly found in people who are unwell, such as those with severe heart and/or lung disease, a severe infection with
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Garcia-Alvarez, Mercedes; Marik, Paul; Bellomo, Rinaldo (April 2014). "Stress hyperlactataemia: present understanding and controversy".
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result of illness but also results from strenuous exercise. The effect on pH is moderated by the presence of respiratory compensation.
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medical condition, medication, or poisoning. The symptoms are generally attributable to these underlying causes, but may include
1164:"Hepatic Failure and Lactic Acidosis Due to Fialuridine (FIAU), an Investigational Nucleoside Analogue for Chronic Hepatitis B" 249: 210: 591:
or dialysis) is difficult, with limited evidence for benefit; it may not be possible to keep up with the lactate production.
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are inhibited, tending to result in a considerable rise of lactate and hydrogen ion concentrations in the rumen fluid. The
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If elevated lactate is present in acute illness, supporting the oxygen supply and blood flow are key initial steps. Some
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Kimberling, C. V. 1988. Jensen and Swift's diseases of sheep. 3rd Ed. Lea & Fibiger, Philadelphia. 394 pp.
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Boyd, JH; Walley, KR (Aug 2008). "Is there a role for sodium bicarbonate in treating lactic acidosis from shock?".
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may be used. The prognosis of lactic acidosis depends largely on the underlying cause; in some situations (such as
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Van Soest, P. J. 1994. Nutritional ecology of the ruminant. 2nd Ed. Cornell Univ. Press, Ithaca. 476 pp.
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solutions to improve the pH (which is associated with increased carbon dioxide generation and may reduce the
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livestock, the cause of clinically serious lactic acidosis is different from the causes described above.
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Kahn, C. M. (ed.) 2005. Merck veterinary manual. 9th Ed. Merck & Co., Inc., Whitehouse Station.
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Impaired delivery of oxygen to cells in the tissues (e.g., from impaired blood flow (hypoperfusion))
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Pfeffer, G; Majamaa, K; Turnbull, DM; Thorburn, D; Chinnery, PF (2012). Chinnery, Patrick F (ed.).
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buried in mud or underwater and do not resurface for the entire winter. As a result, they rely on
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Darmon, Michael; Malak, Sandra; Guichard, Isabelle; Schlemmer, Benoit (July–September 2008).
576:(drugs that augment the blood pressure) are less effective when lactate levels are high, and 1820: 1783: 1744: 1709: 1668: 1566: 1558: 1462: 1425: 1417: 1376: 1368: 1321: 1261: 1216: 1175: 1091: 1075: 1034: 993: 952: 944: 897: 854: 802: 605:
Lactic acidosis caused by inherited mitochondrial disorders (type B3) may be treated with a
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Acid-base disturbances such as lactic acidosis are typically first assessed using
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Son, Hee-Won; Park, Se-Hun; Cho, Hyun-Oh; Shin, Yong-Joon; Son, Jang-Ho (2016).
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Kraut, Jeffrey A.; Madias, Nicolaos E. (11 December 2014). "Lactic Acidosis".
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The diagnosis is made on biochemical analysis of blood (often initially on
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Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes
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Type A: Decreased tissue oxygenation (e.g., from decreased blood flow)
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Seymour R. S.; Webb G. J. W.; Bennett A. F.; Bradford D. F. (1987).
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Journal of the Korean Association of Oral and Maxillofacial Surgeons
476:. In addition, pyruvate generated from lactate can be oxidized to 437:
D-lactic acidosis due to intestinal bacterial flora production in
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Pugh, D. G. 2002. Sheep and goat medicine. Saunders. 468 pp.
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DeFronzo, R; Fleming, GA; Chen, K; Bicsak, TA (February 2016).
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spp. (producing lactate and hydrogen ions) are favored, and
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Fimognari, F. L.; Pastorelli, R.; Incalzi, R. A. (2006).
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The several different causes of lactic acidosis include:
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classification categorizes causes of lactic acidosis as:
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Lactic acidosis is typically the result of an underlying
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Stacpoole, PW; Kurtz, TL; Han, Z; Langaee, T (2008).
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Journal of Neurology, Neurosurgery & Psychiatry
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Clinical and biochemical aspects of lactic acidosis
587:Direct removal of lactate from the body (e.g. with 56: 35: 788: 786: 187:. Symptoms in humans include all those of typical 151:B1: Underlying diseases (sometimes causing type A) 1598: 1596: 1594: 1592: 1590: 784: 782: 780: 778: 776: 774: 772: 770: 768: 766: 1638: 1636: 1540: 1538: 1536: 931:Shah, AD; Wood, DM; Dargan, PI (January 2011). 102:(laboured and deep), and generalised weakness. 1770:Dennis, SM; Nagaraja, TG; Bartley, EE (1981). 1509:Wildlife Management: Crocodiles and Alligators 1287:Goldman, Lee; Schafer, Andrew (May 11, 2015). 285:carried a much higher risk of lactic acidosis. 1981: 8: 1657:"Bovine acidosis: implications on laminitis" 1650: 1648: 455:, in which the molecule is broken down into 125:), it indicates an increased risk of death. 1626: 1624: 1622: 1612: 1610: 1608: 1410:The Cochrane Database of Systematic Reviews 745:Woods, Hubert Frank; Cohen, Robert (1976). 613:(DCA), although this may be complicated by 2009: 1988: 1974: 1966: 1840: 1511:. 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Oxford: Blackwell Scientific. 319:Abacavir/dolutegravir/lamivudine 314:reverse-transcriptase inhibitors 230:Glucose-6-phosphatase deficiency 213:, or nongenetic deficiencies of 1222:10.1590/S0103-507X2008000300011 1168:New England Journal of Medicine 795:New England Journal of Medicine 451:Glucose metabolism begins with 250:Pyruvate carboxylase deficiency 211:multiple carboxylase deficiency 1698:"Acidosis in cattle: a review" 1422:10.1002/14651858.CD004426.pub3 1361:Advanced Drug Delivery Reviews 617:and has a weak evidence base. 504:is highly active (e.g. severe 403:Regional hypoperfusion (e.g., 220:Diabetes mellitus and deafness 154:B2: Medication or intoxication 1: 1266:10.1016/S2213-8587(13)70154-2 999:10.1016/j.metabol.2015.10.014 902:10.1080/14740338.2017.1335305 890:Expert Opinion on Drug Safety 179:due to another cause, severe 1825:10.1016/0301-6226(76)90028-2 1563:10.1113/jphysiol.2002.024729 1326:10.1097/MCC.0b013e3283069d5c 1080:10.5125/jkaoms.2016.42.5.295 1545:Jackson, Donald C. 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Index

Acidosis, lactic

L-(+)-lactic acid
Specialty
Endocrinology
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acute
chronic
nausea
vomiting
Kussmaul breathing
arterial blood gas
hemofiltration
mitochondrial disease
dichloroacetate
severe infections
Cohen
Woods
Inborn error of metabolism
sepsis
systemic inflammatory response syndrome
physical trauma
depletion of body fluids
metabolic acidosis
Biotinidase deficiency
multiple carboxylase deficiency
biotin
Diabetes mellitus and deafness
Fructose 1,6-bisphosphatase deficiency
Glucose-6-phosphatase deficiency

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