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acidosis
renal tubule Acidosis
MedlinePlus
Medical Encyclopedia: Metabolic acidosis
Most symptoms are caused by the disease or condition that is causing the metabolic Acidosis. Metabolic Acidosis itself usually causes rapid breathing. Confusion or lethargy may also occur.
Renal Tubular Acidosis
To diagnose RTA, your doctor will check the acid-base balance in samples of your blood and urine. If the blood is more acidic than it should be and the urine less acidic than it should be, RTA may be the reason, but additional information is needed first to rule out other causes. If RTA is suspected, additional information about the sodium, potassium, and chloride levels in the urine and the potassium level in the blood will help identify which of the three types of RTA you have. In all cases, the first goal of therapy is to neutralize acid in the blood, but different treatments may be needed to address the different underlying causes of Acidosis.
Acidosis - Glossary Entry - Genetics Home Reference
Acidosis
diabetic acidosis
complication of diabetes resulting from severe insulin deficiency coupled with an absolute or relative increase in glucagon concentration; metabolic Acidosis is caused by the breakdown of adipose stores and resulting increased levels of free fatty acids; glucagon accelerates the oxidation of the free fatty acids producing excess ketone bodies (ketosis).
Definition of metabolic acidosis - NCI Dictionary of Cancer Terms
metabolic Acidosis
Lactic acidosis - Glossary Entry - Genetics Home Reference
Acidosis caused by accumulation of lactic acid more rapidly than it can be metabolized. It may occur spontaneously or in association with diseases such as diabetes mellitus, leukemia, or liver failure.
Unmeasured anions in metabolic acidosis: unravelling the mystery
Many studies have highlighted the presence of unmeasured anions in critically ill patients with metabolic Acidosis, although few have been successful in addressing their chemical nature. The prognostic significance of unmeasured anions is also a source of debate but recent studies seem to suggest some predictive ability [ 30 , 31 ]. Certainly, the study from Dondorp and colleagues [ 30 ] supports this view, although the area under receiver operator curve for strong ion gap toward mortality was just 0.73. However, all other predictors also had values 0.8. Interestingly, recent studies on the primary patho-physiological events of malarial infection in animals revealed up-regulation of transcription of genes that control host glycolysis [ 32 ]. One may speculate that the unmeasured anions noted in severe malaria may, therefore, be related to intermediary metabolism, in keeping with our studies. Other workers have demonstrated the presence of organic acids commonly associated with intermediary metabolism under various conditions. Tricarboxylic acids have been detected in human urine [ 33 ] and various organic acids detected in the haemofiltrate of patients with acute renal failure where the presence of elevated citrate levels was loosely associated with a worse prognosis [ 34 ]. Furthermore, citrate, malate and cis-aconitate have been detected in patients with metabolic Acidosis ascribed to salicylate poisoning [ 35 ].
MedlinePlus
Medical Encyclopedia: Acidosis
The kidneys and lungs maintain the body's acid/ base (pH) balance. Acidosis occurs when acid builds up or bicarbonate (a base) is lost. The major categories of Acidosis are respiratory Acidosis and metabolic Acidosis .
Energy Citations Database (ECD) - - Document #7026638
The decrease in myocardial contractility during ischemia, hypoxia, and extracellular Acidosis has been attributed to intracellular Acidosis.^Previous studies of the relationship between pH and contractile state have utilized respiratory or metabolic Acidosis to alter intracellular pH.^The authors developed a model in the working perfused rat heart to study the effects of intracellular Acidosis with normal external pH and optimal O{sub 2} delivery.^Intracellular pH and high-energy phosphates were monitored by {sup 31}P nuclear magnetic resonance spectroscopy.^Hearts were perfused to a steady state with a medium containing 10 mM NH{sub 4}Cl.^Acidosis induced a substantial decrease in aortic flow and stroke volume which was associated with little change in peak systolic pressure.^It was concluded that (1) for the same intracellular Acidosis the influence on tension development was more pronounced with a combined extra- and intracellular Acidosis than with an isolated intracellular Acidosis, and (2) stroke volume at constant preload was impaired by intracellular Acidosis even though changes in developed pressure were minimal.^These observations suggest that isolated intracellular Acidosis has adverse effects on diastolic compliance and/ or relaxation.
Lactic Acidosis Traced to Thiamine Deficiency Related to Nationwide Shortage of Multivitamins for Total Parenteral Nutrition -- United States, 1997
Attempts to introduce clear liquids orally on February 7 and 8 were unsuccessful because of persistent severe anorexia, nausea, and vomiting. On February 10, an upper gastrointestinal barium imaging study revealed delayed transit time, but no mechanical obstruction. During February 10-22, TPN was continued without MVIs. On February 22, the patient was lethargic and weak, and abnormal laboratory findings included severe Acidosis (pH 6.87 {normal: 7.35-7.45}; HCO3, 5 mEq/ L {normal: 24-28 mEq/ L}; pCO2, 28 mm Hg {normal: 35-45 mm Hg}; pO2, 131 mm Hg {normal: 80-100 mm Hg}; and base excess, -13 mEq/ L), glucose level of 570 mg/ dL (normal: 65-110 mg/ dL), and serum lactic acid of 16 mmol/ L (normal: 0.8-2.5 mmol/ L); serum ketones were negative. Lactic Acidosis of unknown etiology was diagnosed, and broad-spectrum antimicrobials were initiated after appropriate cultures were obtained. During the next 8 hours, 600 mEq/ L of bicarbonate was administered with only modest elevation of pH (to 7.20) and no change in base excess (-16.2 mEq/ L). Because the patient's clinical condition continued to deteriorate, an exploratory laparotomy was performed; however, no focus of infection or bowel necrosis was found. An analysis for serum thiamine measured the lowest detectable level of 0.2 mg/ dL (normal: 1.1-1.6 mg/ dL), and 400 mg of thiamine was administered intravenously. Two hours later, a blood gas specimen contained a serum pH of 7.50 and an HCO3 of 11.3 mEq/ L. Acid/ base and clinical status improved; a second dose of 400 mg thiamine was administered intravenously, and pH, pCO2, and HCO3 levels returned to normal. Case 2
Search of: "Acidosis" - List Results - ClinicalTrials.gov
Ketosis Prone Diabetes; Diabetic Ketoacidosis; Severe Hyperglycemia
Renal tubular acidosis, distal, autosomal recessive
The Online Mendelian Inheritance in Man (OMIM) database contains genetics resources that discuss Renal tubular Acidosis, distal, autosomal recessive. Click on the link to go to OMIM and review these resources.
Search of: "Acidosis, Lactic" - List Results - ClinicalTrials.gov
Phase III Randomized Study of Sodium Dichloroacetate in Children With Congenital Lactic Acidosis
Definition of renal tubular acidosis - NCI Dictionary of Cancer Terms
renal tubular Acidosis
Osteopetrosis with renal tubular acidosis
The Online Mendelian Inheritance in Man (OMIM) database contains genetics resources that discuss Osteopetrosis with renal tubular Acidosis. Click on the link to go to OMIM and review these resources.
DNR - Corn Toxicity
A change from a natural diet of high fiber woody browse to low fiber high carbohydrate foods initiates the disease. The severity of the illness depends on the type of grain (ground or whole), previous exposure of the animal to the grain, the amount of grain consumed, the animal's nutritional state and physical condition, and the microflora present. Ingestion of toxic amounts of corn are followed within 2 to 6 hours by a change in the microbial population in the rumen. The number of gram-positive bacteria ( Streptococcus sp. ) increase markedly (replacing the normally abundant gram-negative bacteria), thereby producing large quantities of lactic acid. This results in the rumen pH falling to or below 5, destroying protozoa, cellulolytic organisms, and lactate utilizing organisms, and reducing rumen mobility. Chemical rumenitis and absorption result in lactic Acidosis. The lactic acid and lactate build-up cause excessive quantities of fluid to move into the rumen, causing dehydration.
Base administration or fluid bolus for preventing morbidity and mortality in preterm infants with metabolic acidosis
Similar concerns about the lack of evidence of benefit and potential for harm have been raised about the use of infusion of a fluid bolus in treating preterm infants with metabolic Acidosis or other evidence of systemic underperfusion ( Hope 1998 ). There is some biological plausibility that a fluid bolus may improve organ perfusion in infants with hypovolaemia. However, in the absence of a clear precipitating event such as haemorrhage, hypovolaemia is probably a rare cause of metabolic Acidosis in preterm infants. Because systemic underperfusion and hypovolaemia are very difficult to assess clinically many infants may receive treatment with a fluid bolus inappropriately. A Cochrane review found insufficient evidence that routine early volume expansion with blood products or crystalloid solutions prevents morbidity and mortality in very preterm infants ( Osborn 2004 ). In this review, we did not find any randomised controlled trials that compared the effect of treatment with fluid bolus versus no treatment in preterm infants with metabolic Acidosis. Dixon 1999 compared base infusion with fluid bolus and found some evidence (of borderline clinical significance) that base infusion corrected metabolic Acidosis more effectively than fluid bolus. This trial specifically excluded infants with evidence of hypotension from participating.
Acidosis
Acidosis
Lactate versus non-lactate metabolic acidosis: a retrospective outcome evaluation of critically ill patients
This study has several limitations. First, as a retrospective study, our database is limited to the variables that were collected for clinical management, and some patients with metabolic Acidosis may have been excluded because of missing data. However, these were the data available to clinicians and our study demonstrates that a significant number of patients suspected of having lactic Acidosis clinically do in fact have other forms of metabolic Acidosis. Second, we could not control for severity of illness between groups. Severity of illness scores (for example Acute Physiology and Chronic Health Evaluation (APACHE)) were recorded only on admission to ICU and only in a subset of patients. Several patients had their highest lactate levels several days into their stay in ICU. However, the use of severity of illness scores are potentially misleading because metabolic Acidosis itself might lead to worsening disease severity. Indeed, most severity scoring systems take into account acid base variables and/ or lactate. Thus, for our model we included age as covariate. We also report the admission diagnostic category in Table 2 . The nature of our database (laboratory values) also limited our logistic regression model. Ideally we would have included treatment variables (saline and other resuscitation fluid) as well as other clinical variables (hemodynamics). Another limitation involved our initial selection process. The 'suspicion of lactic Acidosis' excluded several patients in whom a metabolic Acidosis may have been present for other reasons but was not suspected. The categories of metabolic Acidosis were used to describe the predominating anion. Rather than using an arbitrary definition of hyperchloremic metabolic Acidosis that relies on an absolute value of chloride, we first eliminated all other causes of what has been traditionally classified as an anion gap metabolic Acidosis (SIG or lactate). Our classification scheme leaves open the possibility that a combined la
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