Acidosis
Acidosis, Lactic
Acidosis, Renal Tubular
Acid-Base Equilibrium
Bicarbonates
Hydrogen-Ion Concentration
Sodium Bicarbonate
Ammonium Chloride
MELAS Syndrome
Carbon Dioxide
Diabetic Ketoacidosis
Hypercapnia
Alkalosis, Respiratory
Lactic Acid
Potassium Citrate
Phenformin
Sodium-Hydrogen Antiporter
Ammonia
Sodium-Bicarbonate Symporters
Acids
Hydrochloric Acid
Hypokalemia
Hyperkalemia
Fanconi Syndrome
RNA, Transfer, Leu
Acid Sensing Ion Channels
Partial Pressure
Glutaminase
Kidney
Dichloroacetic Acid
Nephrocalcinosis
Rumen
Decreased lactic acidosis and anemia after transfusion of o-raffinose cross-linked and polymerized hemoglobin in severe murine malaria. (1/290)
Severe anemia is a major cause of death in falciparum malaria. Blood transfusion increases survival in humans and in animal models of this disease. Because of logistic constraints and viral contamination of the blood supply, transfusions are frequently not practical in endemic regions. Modified hemoglobin is an effective O2 carrier in hemorrhagic shock. It is free of infectious contamination, may not require refrigeration, and because of its nitric oxide scavenging and small size, may have pharmacologic benefits in malaria. The effects of transfusions of modified hemoglobin in rats with high-grade parasitemia were evaluated. Modified hemoglobin decreased lactic acidosis and corrected anemia as well as transfusions with red blood cells; these findings may correlate with improved survival and suggest a possible proerythropoietic effect. Further study of this novel therapy is warranted. (+info)Incidence of lactic acidosis in metformin users. (2/290)
OBJECTIVE: The purpose of this study was to determine the incidence of lactic acidosis in a geographically defined population of metformin users. RESEARCH DESIGN AND METHODS: The study was based on a historical cohort from the Saskatchewan Health administrative databases. Individuals with a metformin prescription dispensed between 1980 and 1995 inclusive were eligible for the cohort. Person-years of exposure were calculated. Cases were defined by hospital discharge with a diagnosis of acidosis (International Classification of Diseases, Ninth Revision code: 276.2) and confirmation by chart review of a blood lactate level > or = 5 mmol/l. Death registrations of individuals dying within 120 days of a metformin prescription were also reviewed. RESULTS: During the study period, 11,797 residents received one or more metformin prescriptions, resulting in 22,296 person-years of exposure. There were 10 subjects who had hospital discharges with a diagnosis of acidosis. However, primary record review revealed only two cases with laboratory findings of elevated blood lactate levels, for an incidence rate of 9 cases per 100,000 person-years of metformin exposure. In both cases, other factors besides metformin could have contributed to the lactic acidosis. No additional cases were found on review of death registrations. CONCLUSIONS: From 1980 through 1995, the incidence rate of lactic acidosis was 9 per 100,000 person-years (95% CI 0-21) in patients dispensed metformin in Saskatchewan, Canada. This incidence rate was derived from a population with complete ascertainment of hospitalizations and deaths associated with lactic acidosis in metformin users. It is similar to previously published rates based on passive reporting of cases, and it is well below the lactic acidosis rate of 40-64 per 100,000 patient-years in patients prescribed phenformin. (+info)Nuclear DNA origin of mitochondrial complex I deficiency in fatal infantile lactic acidosis evidenced by transnuclear complementation of cultured fibroblasts. (3/290)
We have studied complex I (NADH-ubiquinone reductase) defects of the mitochondrial respiratory chain in 2 infants who died in the neonatal period from 2 different neurological forms of severe neonatal lactic acidosis. Specific and marked decrease in complex I activity was documented in muscle, liver, and cultured skin fibroblasts. Biochemical characterization and study of the genetic origin of this defect were performed using cultured fibroblasts. Immunodetection of 6 nuclear DNA-encoded (20, 23, 24, 30, 49, and 51 kDa) and 1 mitochondrial DNA-encoded (ND1) complex I subunits in fibroblast mitochondria revealed 2 distinct patterns. In 1 patient, complex I contained reduced amounts of the 24- and 51-kDa subunits and normal amounts of all the other investigated subunits. In the second patient, amounts of all the investigated subunits were severely decreased. The data suggest partial or extensive impairment of complex I assembly in both patients. Cell fusion experiments between 143B206 rho degrees cells, fully depleted of mitochondrial DNA, and fibroblasts from both patients led to phenotypic complementation of the complex I defects in mitochondria of the resulting cybrid cells. These results indicate that the complex I defects in the 2 reported cases are due to nuclear gene mutations. (+info)Blood lactate accumulation and muscle deoxygenation during incremental exercise. (4/290)
Near-infrared spectroscopy (NIRS) could allow insights into controversial issues related to blood lactate concentration ([La](b)) increases at submaximal workloads (). We combined, on five well-trained subjects [mountain climbers; peak O(2) consumption (VO(2peak)), 51.0 +/- 4.2 (SD) ml. kg(-1). min(-1)] performing incremental exercise on a cycle ergometer (30 W added every 4 min up to voluntary exhaustion), measurements of pulmonary gas exchange and earlobe [La](b) with determinations of concentration changes of oxygenated Hb (Delta[O(2)Hb]) and deoxygenated Hb (Delta[HHb]) in the vastus lateralis muscle, by continuous-wave NIRS. A "point of inflection" of [La](b) vs. was arbitrarily identified at the lowest [La](b) value which was >0.5 mM lower than that obtained at the following. Total Hb volume (Delta[O(2)Hb + HHb]) in the muscle region of interest increased as a function of up to 60-65% of VO(2 peak), after which it remained unchanged. The oxygenation index (Delta[O(2)Hb - HHb]) showed an accelerated decrease from 60- 65% of VO(2 peak). In the presence of a constant total Hb volume, the observed Delta[O(2)Hb - HHb] decrease indicates muscle deoxygenation (i.e., mainly capillary-venular Hb desaturation). The onset of muscle deoxygenation was significantly correlated (r(2) = 0.95; P < 0.01) with the point of inflection of [La](b) vs., i.e., with the onset of blood lactate accumulation. Previous studies showed relatively constant femoral venous PO(2) levels at higher than approximately 60% of maximal O(2) consumption. Thus muscle deoxygenation observed in the present study from 60-65% of VO(2 peak) could be attributed to capillary-venular Hb desaturation in the presence of relatively constant capillary-venular PO(2) levels, as a consequence of a rightward shift of the O(2)Hb dissociation curve determined by the onset of lactic acidosis. (+info)Hypoxia-activated apoptosis of cardiac myocytes requires reoxygenation or a pH shift and is independent of p53. (5/290)
Ischemia and reperfusion activate cardiac myocyte apoptosis, which may be an important feature in the progression of ischemic heart disease. The relative contributions of ischemia and reperfusion to apoptotic signal transduction have not been established. We report here that severe chronic hypoxia alone does not cause apoptosis of cardiac myocytes in culture. When rapidly contracting cardiac myocytes were exposed to chronic hypoxia, apoptosis occurred only when there was a decrease in extracellular pH ([pH](o)). Apoptosis did not occur when [pH](o) was neutralized. Addition of acidic medium from hypoxic cultures or exogenous lactic acid stimulated apoptosis in aerobic myocytes. Hypoxia-acidosis-mediated cell death was independent of p53: equivalent apoptosis occurred in cardiac myocytes isolated from wild-type and p53 knockout mice, and hypoxia caused no detectable change in p53 abundance or p53-dependent transcription. Reoxygenation of hypoxic cardiac myocytes induced apoptosis in 25-30% of the cells and was also independent of p53 by the same criteria. Finally, equivalent levels of apoptosis, as demonstrated by DNA fragmentation, were induced by ischemia-reperfusion, but not by ischemia alone, of Langendorff-perfused hearts from wild-type and p53 knockout mice. We conclude that acidosis, reoxygenation, and reperfusion, but not hypoxia (or ischemia) alone, are strong stimuli for programmed cell death that is substantially independent of p53. (+info)Actively phosphorylating mitochondria are more resistant to lactic acidosis than inactive mitochondria. (6/290)
Oxidative phosphorylation of isolated rat skeletal muscle mitochondria after exposure to lactic acidosis in either phosphorylating or nonphosphorylating states has been evaluated. Mitochondrial respiration and transmembrane potential (DeltaPsi(m)) were measured with pyruvate and malate as the substrates. The addition of lactic acid decreased the pH of the reaction medium from 7.5 to 6.4. When lactic acid was added to nonphosphorylating mitochondria, the subsequent maximal ADP-stimulated respiration decreased by 27% compared with that under control conditions (P < 0.05), and the apparent Michaelis-Menten constant (K(m)) for ADP decreased to 10 microM vs. 20 microM (P < 0.05) in controls. In contrast, maximal respiration and ADP sensitivity were not affected when mitochondria were exposed to acidosis during active phosphorylation in state 3. Acidosis significantly increased mitochondrial oxygen consumption in state 4 (post-state 3), irrespective of when acidosis was induced. This effect of acidosis was attenuated in the presence of oligomycin. The addition of lactic acid during state 4 respiration decreased DeltaPsi(m) by 19%. The ratio between added ADP and consumed oxygen (P/O) was close to the theoretical value of 3 in all conditions. The addition of potassium lactate during state 3 (i.e., medium pH unchanged) had no effect on the parameters measured. It is concluded that lactic acidosis has different effects when induced on nonphosphorylating vs. actively phosphorylating mitochondria. On the basis of these results, we suggest that the influence of lactic acidosis on muscle aerobic energy production depends on the physiological conditions at the onset of acidity. (+info)A novel deficiency of mitochondrial ATPase of nuclear origin. (7/290)
We report a new type of fatal mitochondrial disorder caused by selective deficiency of mitochondrial ATP synthase (ATPase). A hypotrophic newborn from a consanguineous marriage presented severe lactic acidosis, cardiomegaly and hepatomegaly and died from heart failure after 2 days. The activity of oligomycin-sensitive ATPase was only 31-34% of the control, both in muscle and heart, but the activities of cytochrome c oxidase, citrate synthase and pyruvate dehydrogenase were normal. Electrophoretic and western blot analysis revealed selective reduction of ATPase complex but normal levels of the respiratory chain complexes I, III and IV. The same selective deficiency of ATPase was found in cultured skin fibroblasts which showed similar decreases in ATPase content, ATPase hydrolytic activity and level of substrate-dependent ATP synthesis (20-25, 18 and 29-33% of the control, respectively). Pulse-chase labelling of patient fibroblasts revealed low incorporation of [(35)S]methionine into assembled ATPase complexes, but increased incorporation into immunoprecipitated ATPase subunit beta, which had a very short half-life. In contrast, no difference was found in the size and subunit composition of the assembled and newly produced ATPase complex. Transmitochondrial cybrids prepared from enucleated fibroblasts of the patient and rho degrees cells derived from 143B. TK(-)human osteosarcoma cells fully restored the ATPase activity, ATP synthesis and ATPase content, when compared with control cybrids. Likewise, the pattern of [(35)S]methionine labelling of ATPase was found to be normal in patient cybrids. We conclude that the generalized deficiency of mitochondrial ATPase described is of nuclear origin and is caused by altered biosynthesis of the enzyme. (+info)A missense mutation of cytochrome oxidase subunit II causes defective assembly and myopathy. (8/290)
We report the first missense mutation in the mtDNA gene for subunit II of cytochrome c oxidase (COX). The mutation was identified in a 14-year-old boy with a proximal myopathy and lactic acidosis. Muscle histochemistry and mitochondrial respiratory-chain enzymology demonstrated a marked reduction in COX activity. Immunohistochemistry and immunoblot analyses with COX subunit-specific monoclonal antibodies showed a pattern suggestive of a primary mtDNA defect, most likely involving CO II, for COX subunit II (COX II). mtDNA-sequence analysis demonstrated a novel heteroplasmic T-->A transversion at nucleotide position 7,671 in CO II. This mutation changes a methionine to a lysine residue in the middle of the first N-terminal membrane-spanning region of COX II. The immunoblot studies demonstrated a severe reduction in cross-reactivity, not only for COX II but also for the mtDNA-encoded subunit COX III and for nuclear-encoded subunits Vb, VIa, VIb, and VIc. Steady-state levels of the mtDNA-encoded subunit COX I showed a mild reduction, but spectrophotometric analysis revealed a dramatic decrease in COX I-associated heme a3 levels. These observations suggest that, in the COX protein, a structural association of COX II with COX I is necessary to stabilize the binding of heme a3 to COX I. (+info)Acidosis is a medical condition that occurs when there is an excess accumulation of acid in the body or when the body loses its ability to effectively regulate the pH level of the blood. The normal pH range of the blood is slightly alkaline, between 7.35 and 7.45. When the pH falls below 7.35, it is called acidosis.
Acidosis can be caused by various factors, including impaired kidney function, respiratory problems, diabetes, severe dehydration, alcoholism, and certain medications or toxins. There are two main types of acidosis: metabolic acidosis and respiratory acidosis.
Metabolic acidosis occurs when the body produces too much acid or is unable to eliminate it effectively. This can be caused by conditions such as diabetic ketoacidosis, lactic acidosis, kidney failure, and ingestion of certain toxins.
Respiratory acidosis, on the other hand, occurs when the lungs are unable to remove enough carbon dioxide from the body, leading to an accumulation of acid. This can be caused by conditions such as chronic obstructive pulmonary disease (COPD), asthma, and sedative overdose.
Symptoms of acidosis may include fatigue, shortness of breath, confusion, headache, rapid heartbeat, and in severe cases, coma or even death. Treatment for acidosis depends on the underlying cause and may include medications, oxygen therapy, fluid replacement, and dialysis.
Lactic acidosis is a medical condition characterized by an excess accumulation of lactic acid in the body. Lactic acid is a byproduct produced in the muscles and other tissues during periods of low oxygen supply or increased energy demand. Under normal circumstances, lactic acid is quickly metabolized and cleared from the body. However, when the production of lactic acid exceeds its clearance, it can lead to a state of acidosis, where the pH of the blood becomes too acidic.
Lactic acidosis can be caused by several factors, including:
* Prolonged exercise or strenuous physical activity
* Severe illness or infection
* Certain medications, such as metformin and isoniazid
* Alcoholism
* Hypoxia (low oxygen levels) due to lung disease, heart failure, or anemia
* Inherited metabolic disorders that affect the body's ability to metabolize lactic acid
Symptoms of lactic acidosis may include rapid breathing, fatigue, muscle weakness, nausea, vomiting, and abdominal pain. Severe cases can lead to coma, organ failure, and even death. Treatment typically involves addressing the underlying cause of the condition and providing supportive care, such as administering intravenous fluids and bicarbonate to help restore normal pH levels.
Respiratory acidosis is a medical condition that occurs when the lungs are not able to remove enough carbon dioxide (CO2) from the body, leading to an increase in the amount of CO2 in the bloodstream and a decrease in the pH of the blood. This can happen due to various reasons such as chronic lung diseases like emphysema or COPD, severe asthma attacks, neuromuscular disorders that affect breathing, or when someone is not breathing deeply or frequently enough, such as during sleep apnea or drug overdose.
Respiratory acidosis can cause symptoms such as headache, confusion, shortness of breath, and in severe cases, coma and even death. Treatment for respiratory acidosis depends on the underlying cause but may include oxygen therapy, bronchodilators, or mechanical ventilation to help support breathing.
Renal tubular acidosis (RTA) is a medical condition that occurs when the kidneys are unable to properly excrete acid into the urine, leading to an accumulation of acid in the bloodstream. This results in a state of metabolic acidosis.
There are several types of RTA, but renal tubular acidosis type 1 (also known as distal RTA) is characterized by a defect in the ability of the distal tubules to acidify the urine, leading to an inability to lower the pH of the urine below 5.5, even in the face of metabolic acidosis. This results in a persistently alkaline urine, which can lead to calcium phosphate stones and bone demineralization.
Type 1 RTA is often caused by inherited genetic defects, but it can also be acquired due to various kidney diseases, drugs, or autoimmune disorders. Symptoms of type 1 RTA may include fatigue, weakness, muscle cramps, decreased appetite, and vomiting. Treatment typically involves alkali therapy to correct the acidosis and prevent complications.
Acid-base equilibrium refers to the balance between the concentration of acids and bases in a solution, which determines its pH level. In a healthy human body, maintaining acid-base equilibrium is crucial for proper cellular function and homeostasis.
The balance is maintained by several buffering systems in the body, including the bicarbonate buffer system, which helps to regulate the pH of blood. This system involves the reaction between carbonic acid (a weak acid) and bicarbonate ions (a base) to form water and carbon dioxide.
The balance between acids and bases is carefully regulated by the body's respiratory and renal systems. The lungs control the elimination of carbon dioxide, a weak acid, through exhalation, while the kidneys regulate the excretion of hydrogen ions and the reabsorption of bicarbonate ions.
When the balance between acids and bases is disrupted, it can lead to acid-base disorders such as acidosis (excessive acidity) or alkalosis (excessive basicity). These conditions can have serious consequences on various organ systems if left untreated.
Bicarbonates, also known as sodium bicarbonate or baking soda, is a chemical compound with the formula NaHCO3. In the context of medical definitions, bicarbonates refer to the bicarbonate ion (HCO3-), which is an important buffer in the body that helps maintain normal pH levels in blood and other bodily fluids.
The balance of bicarbonate and carbonic acid in the body helps regulate the acidity or alkalinity of the blood, a condition known as pH balance. Bicarbonates are produced by the body and are also found in some foods and drinking water. They work to neutralize excess acid in the body and help maintain the normal pH range of 7.35 to 7.45.
In medical testing, bicarbonate levels may be measured as part of an electrolyte panel or as a component of arterial blood gas (ABG) analysis. Low bicarbonate levels can indicate metabolic acidosis, while high levels can indicate metabolic alkalosis. Both conditions can have serious consequences if not treated promptly and appropriately.
Hydrogen-ion concentration, also known as pH, is a measure of the acidity or basicity of a solution. It is defined as the negative logarithm (to the base 10) of the hydrogen ion activity in a solution. The standard unit of measurement is the pH unit. A pH of 7 is neutral, less than 7 is acidic, and greater than 7 is basic.
In medical terms, hydrogen-ion concentration is important for maintaining homeostasis within the body. For example, in the stomach, a high hydrogen-ion concentration (low pH) is necessary for the digestion of food. However, in other parts of the body such as blood, a high hydrogen-ion concentration can be harmful and lead to acidosis. Conversely, a low hydrogen-ion concentration (high pH) in the blood can lead to alkalosis. Both acidosis and alkalosis can have serious consequences on various organ systems if not corrected.
Sodium bicarbonate, also known as baking soda, is a chemical compound with the formula NaHCO3. It is a white solid that is crystalline but often appears as a fine powder. It has a slightly salty, alkaline taste and is commonly used in cooking as a leavening agent.
In a medical context, sodium bicarbonate is used as a medication to treat conditions caused by high levels of acid in the body, such as metabolic acidosis. It works by neutralizing the acid and turning it into a harmless salt and water. Sodium bicarbonate can be given intravenously or orally, depending on the severity of the condition being treated.
It is important to note that sodium bicarbonate should only be used under the supervision of a healthcare professional, as it can have serious side effects if not used properly. These may include fluid buildup in the body, electrolyte imbalances, and an increased risk of infection.
Alkalosis is a medical condition that refers to an excess of bases or a decrease in the concentration of hydrogen ions (H+) in the blood, leading to a higher than normal pH level. The normal range for blood pH is typically between 7.35 and 7.45. A pH above 7.45 indicates alkalosis.
Alkalosis can be caused by several factors, including:
1. Metabolic alkalosis: This type of alkalosis occurs due to an excess of bicarbonate (HCO3-) in the body, which can result from conditions such as excessive vomiting, hyperventilation, or the use of certain medications like diuretics.
2. Respiratory alkalosis: This form of alkalosis is caused by a decrease in carbon dioxide (CO2) levels in the blood due to hyperventilation or other conditions that affect breathing, such as high altitude, anxiety, or lung disease.
Symptoms of alkalosis can vary depending on its severity and underlying cause. Mild alkalosis may not produce any noticeable symptoms, while severe cases can lead to muscle twitching, cramps, tremors, confusion, and even seizures. Treatment for alkalosis typically involves addressing the underlying cause and restoring the body's normal pH balance through medications or other interventions as necessary.
Ammonium chloride is an inorganic compound with the formula NH4Cl. It is a white crystalline salt that is highly soluble in water and can be produced by combining ammonia (NH3) with hydrochloric acid (HCl). Ammonium chloride is commonly used as a source of hydrogen ions in chemical reactions, and it has a variety of industrial and medical applications.
In the medical field, ammonium chloride is sometimes used as a expectorant to help thin and loosen mucus in the respiratory tract, making it easier to cough up and clear from the lungs. It may also be used to treat conditions such as metabolic alkalosis, a condition characterized by an excess of base in the body that can lead to symptoms such as confusion, muscle twitching, and irregular heartbeat.
However, it is important to note that ammonium chloride can have side effects, including stomach upset, nausea, vomiting, and diarrhea. It should be used under the guidance of a healthcare professional and should not be taken in large amounts or for extended periods of time without medical supervision.
Mitochondrial Encephalomyopathy, Lactic Acidosis, and Stroke-like episodes (MELAS) syndrome is a rare inherited mitochondrial disorder that affects the body's energy production mechanisms. It is characterized by a combination of symptoms including recurrent headaches, vomiting, seizures, vision loss, hearing impairment, muscle weakness, and stroke-like episodes affecting primarily young adults.
The condition is caused by mutations in the mitochondrial DNA (mtDNA), most commonly the A3243G point mutation in the MT-TL1 gene. The symptoms of MELAS syndrome can vary widely among affected individuals, even within the same family, due to the complex inheritance pattern of mtDNA.
MELAS syndrome is typically diagnosed based on a combination of clinical features, laboratory tests, and genetic testing. Treatment is supportive and aimed at managing individual symptoms as they arise.
Carbon dioxide (CO2) is a colorless, odorless gas that is naturally present in the Earth's atmosphere. It is a normal byproduct of cellular respiration in humans, animals, and plants, and is also produced through the combustion of fossil fuels such as coal, oil, and natural gas.
In medical terms, carbon dioxide is often used as a respiratory stimulant and to maintain the pH balance of blood. It is also used during certain medical procedures, such as laparoscopic surgery, to insufflate (inflate) the abdominal cavity and create a working space for the surgeon.
Elevated levels of carbon dioxide in the body can lead to respiratory acidosis, a condition characterized by an increased concentration of carbon dioxide in the blood and a decrease in pH. This can occur in conditions such as chronic obstructive pulmonary disease (COPD), asthma, or other lung diseases that impair breathing and gas exchange. Symptoms of respiratory acidosis may include shortness of breath, confusion, headache, and in severe cases, coma or death.
An acid-base imbalance refers to a disturbance in the normal balance of acids and bases in the body, which can lead to serious health consequences. The body maintains a delicate balance between acids and bases, which is measured by the pH level of the blood. The normal range for blood pH is between 7.35 and 7.45, with a pH below 7.35 considered acidic and a pH above 7.45 considered basic or alkaline.
Acid-base imbalances can occur due to various factors such as lung or kidney disease, diabetes, severe infections, certain medications, and exposure to toxins. The two main types of acid-base imbalances are acidosis (excess acid in the body) and alkalosis (excess base in the body).
Acidosis can be further classified into respiratory acidosis (caused by impaired lung function or breathing difficulties) and metabolic acidosis (caused by an accumulation of acid in the body due to impaired kidney function, diabetes, or other conditions).
Alkalosis can also be classified into respiratory alkalosis (caused by hyperventilation or excessive breathing) and metabolic alkalosis (caused by excessive loss of stomach acid or an excess intake of base-forming substances).
Symptoms of acid-base imbalances may include confusion, lethargy, shortness of breath, rapid heartbeat, nausea, vomiting, and muscle weakness. If left untreated, these conditions can lead to serious complications such as coma, seizures, or even death. Treatment typically involves addressing the underlying cause of the imbalance and may include medications, oxygen therapy, or fluid and electrolyte replacement.
Diabetic ketoacidosis (DKA) is a serious metabolic complication characterized by the triad of hyperglycemia, metabolic acidosis, and increased ketone bodies. It primarily occurs in individuals with diabetes mellitus type 1, but it can also be seen in some people with diabetes mellitus type 2, particularly during severe illness or surgery.
The condition arises when there is a significant lack of insulin in the body, which impairs the ability of cells to take up glucose for energy production. As a result, the body starts breaking down fatty acids to produce energy, leading to an increase in ketone bodies (acetoacetate, beta-hydroxybutyrate, and acetone) in the bloodstream. This process is called ketosis.
In DKA, the excessive production of ketone bodies results in metabolic acidosis, which is characterized by a lower than normal pH level in the blood (< 7.35) and an elevated serum bicarbonate level (< 18 mEq/L). The hyperglycemia in DKA is due to both increased glucose production and decreased glucose utilization by cells, which can lead to severe dehydration and electrolyte imbalances.
Symptoms of diabetic ketoacidosis include excessive thirst, frequent urination, nausea, vomiting, abdominal pain, fatigue, fruity breath odor, and altered mental status. If left untreated, DKA can progress to coma and even lead to death. Treatment typically involves administering insulin, fluid replacement, and electrolyte management in a hospital setting.
Lactates, also known as lactic acid, are compounds that are produced by muscles during intense exercise or other conditions of low oxygen supply. They are formed from the breakdown of glucose in the absence of adequate oxygen to complete the full process of cellular respiration. This results in the production of lactate and a hydrogen ion, which can lead to a decrease in pH and muscle fatigue.
In a medical context, lactates may be measured in the blood as an indicator of tissue oxygenation and metabolic status. Elevated levels of lactate in the blood, known as lactic acidosis, can indicate poor tissue perfusion or hypoxia, and may be seen in conditions such as sepsis, cardiac arrest, and severe shock. It is important to note that lactates are not the primary cause of acidemia (low pH) in lactic acidosis, but rather a marker of the underlying process.
Hypercapnia is a state of increased carbon dioxide (CO2) concentration in the blood, typically defined as an arterial CO2 tension (PaCO2) above 45 mmHg. It is often associated with conditions that impair gas exchange or eliminate CO2 from the body, such as chronic obstructive pulmonary disease (COPD), severe asthma, respiratory failure, or certain neuromuscular disorders. Hypercapnia can cause symptoms such as headache, confusion, shortness of breath, and in severe cases, it can lead to life-threatening complications such as respiratory acidosis, coma, and even death if not promptly treated.
Respiratory alkalosis is a medical condition that occurs when there is an excess base (bicarbonate) and/or a decrease in carbon dioxide in the body. This leads to an increase in pH level of the blood, making it more alkaline than normal. Respiratory alkalosis is usually caused by conditions that result in hyperventilation, such as anxiety, lung disease, or high altitude. It can also be caused by certain medications and medical procedures. Symptoms of respiratory alkalosis may include lightheadedness, confusion, and tingling in the fingers and toes. Treatment typically involves addressing the underlying cause of the condition.
Lactic acid, also known as 2-hydroxypropanoic acid, is a chemical compound that plays a significant role in various biological processes. In the context of medicine and biochemistry, lactic acid is primarily discussed in relation to muscle metabolism and cellular energy production. Here's a medical definition for lactic acid:
Lactic acid (LA): A carboxylic acid with the molecular formula C3H6O3 that plays a crucial role in anaerobic respiration, particularly during strenuous exercise or conditions of reduced oxygen availability. It is formed through the conversion of pyruvate, catalyzed by the enzyme lactate dehydrogenase (LDH), when there is insufficient oxygen to complete the final step of cellular respiration in the Krebs cycle. The accumulation of lactic acid can lead to acidosis and muscle fatigue. Additionally, lactic acid serves as a vital intermediary in various metabolic pathways and is involved in the production of glucose through gluconeogenesis in the liver.
Blood gas analysis is a medical test that measures the levels of oxygen and carbon dioxide in the blood, as well as the pH level, which indicates the acidity or alkalinity of the blood. This test is often used to evaluate lung function, respiratory disorders, and acid-base balance in the body. It can also be used to monitor the effectiveness of treatments for conditions such as chronic obstructive pulmonary disease (COPD), asthma, and other respiratory illnesses. The analysis is typically performed on a sample of arterial blood, although venous blood may also be used in some cases.
Potassium citrate is a medication and dietary supplement that contains potassium and citrate. Medically, it is used to treat and prevent kidney stones, as well as to manage metabolic acidosis in people with chronic kidney disease. Potassium citrate works by increasing the pH of urine, making it less acidic, which can help to dissolve certain types of kidney stones and prevent new ones from forming. It is also used as an alkalizing agent in the treatment of various conditions that cause acidosis.
In addition to its medical uses, potassium citrate is also found naturally in some fruits and vegetables, such as oranges, grapefruits, lemons, limes, and spinach. It is often used as a food additive and preservative, and can be found in a variety of processed foods and beverages.
It's important to note that taking too much potassium citrate can lead to high levels of potassium in the blood, which can be dangerous. Therefore, it is important to follow the dosage instructions carefully and talk to your doctor before taking this medication if you have any medical conditions or are taking any other medications.
Phenformin is a medication that was previously used to treat type 2 diabetes. It belongs to a class of drugs called biguanides, which work to decrease the amount of glucose produced by the liver and increase the body's sensitivity to insulin. However, phenformin was associated with an increased risk of lactic acidosis, a potentially life-threatening condition characterized by an excessive buildup of lactic acid in the bloodstream. As a result, it is no longer available or recommended for use in most countries, including the United States.
A Sodium-Hydrogen Antiporter (NHA) is a type of membrane transport protein that exchanges sodium ions (Na+) and protons (H+) across a biological membrane. It is also known as a Na+/H+ antiporter or exchanger. This exchange mechanism plays a crucial role in regulating pH, cell volume, and intracellular sodium concentration within various cells and organelles, including the kidney, brain, heart, and mitochondria.
In general, NHA transporters utilize the energy generated by the electrochemical gradient of sodium ions across a membrane to drive the uphill transport of protons from inside to outside the cell or organelle. This process helps maintain an optimal intracellular pH and volume, which is essential for proper cellular function and homeostasis.
There are several isoforms of Sodium-Hydrogen Antiporters found in different tissues and organelles, each with distinct physiological roles and regulatory mechanisms. Dysfunction or alterations in NHA activity have been implicated in various pathophysiological conditions, such as hypertension, heart failure, neurological disorders, and cancer.
Ammonia is a colorless, pungent-smelling gas with the chemical formula NH3. It is a compound of nitrogen and hydrogen and is a basic compound, meaning it has a pH greater than 7. Ammonia is naturally found in the environment and is produced by the breakdown of organic matter, such as animal waste and decomposing plants. In the medical field, ammonia is most commonly discussed in relation to its role in human metabolism and its potential toxicity.
In the body, ammonia is produced as a byproduct of protein metabolism and is typically converted to urea in the liver and excreted in the urine. However, if the liver is not functioning properly or if there is an excess of protein in the diet, ammonia can accumulate in the blood and cause a condition called hyperammonemia. Hyperammonemia can lead to serious neurological symptoms, such as confusion, seizures, and coma, and is treated by lowering the level of ammonia in the blood through medications, dietary changes, and dialysis.
Sodium-bicarbonate symporters, also known as sodium bicarbonate co-transporters, are membrane transport proteins that facilitate the movement of both sodium ions (Na+) and bicarbonate ions (HCO3-) across the cell membrane in the same direction. These transporters play a crucial role in maintaining acid-base balance in the body by regulating the concentration of bicarbonate ions, which is an important buffer in the blood and other bodily fluids.
The term "symporter" refers to the fact that these proteins transport two or more different molecules or ions in the same direction across a membrane. In this case, sodium-bicarbonate symporters co-transport one sodium ion and one bicarbonate ion together, usually using a concentration gradient of sodium to drive the uptake of bicarbonate.
These transporters are widely expressed in various tissues, including the kidneys, where they help reabsorb bicarbonate ions from the urine back into the bloodstream, and the gastrointestinal tract, where they contribute to the absorption of sodium and bicarbonate from food and drink. Dysfunction of sodium-bicarbonate symporters has been implicated in several diseases, including renal tubular acidosis and hypertension.
In medical terms, acids refer to a class of chemicals that have a pH less than 7 and can donate protons (hydrogen ions) in chemical reactions. In the context of human health, acids are an important part of various bodily functions, such as digestion. However, an imbalance in acid levels can lead to medical conditions. For example, an excess of hydrochloric acid in the stomach can cause gastritis or peptic ulcers, while an accumulation of lactic acid due to strenuous exercise or decreased blood flow can lead to muscle fatigue and pain.
Additionally, in clinical laboratory tests, certain substances may be tested for their "acidity" or "alkalinity," which is measured using a pH scale. This information can help diagnose various medical conditions, such as kidney disease or diabetes.
Hydrochloric acid, also known as muriatic acid, is not a substance that is typically found within the human body. It is a strong mineral acid with the chemical formula HCl. In a medical context, it might be mentioned in relation to gastric acid, which helps digest food in the stomach. Gastric acid is composed of hydrochloric acid, potassium chloride and sodium chloride dissolved in water. The pH of hydrochloric acid is very low (1-2) due to its high concentration of H+ ions, making it a strong acid. However, it's important to note that the term 'hydrochloric acid' does not directly refer to a component of human bodily fluids or tissues.
Hypokalemia is a medical condition characterized by abnormally low potassium levels in the blood, specifically when the concentration falls below 3.5 milliequivalents per liter (mEq/L). Potassium is an essential electrolyte that helps regulate heart function, nerve signals, and muscle contractions.
Hypokalemia can result from various factors, including inadequate potassium intake, increased potassium loss through the urine or gastrointestinal tract, or shifts of potassium between body compartments. Common causes include diuretic use, vomiting, diarrhea, certain medications, kidney diseases, and hormonal imbalances.
Mild hypokalemia may not cause noticeable symptoms but can still affect the proper functioning of muscles and nerves. More severe cases can lead to muscle weakness, fatigue, cramps, paralysis, heart rhythm abnormalities, and in rare instances, respiratory failure or cardiac arrest. Treatment typically involves addressing the underlying cause and replenishing potassium levels through oral or intravenous (IV) supplementation, depending on the severity of the condition.
Hyperkalemia is a medical condition characterized by an elevated level of potassium (K+) in the blood serum, specifically when the concentration exceeds 5.0-5.5 mEq/L (milliequivalents per liter). Potassium is a crucial intracellular ion that plays a significant role in various physiological processes, including nerve impulse transmission, muscle contraction, and heart rhythm regulation.
Mild to moderate hyperkalemia might not cause noticeable symptoms but can still have harmful effects on the body, particularly on the cardiovascular system. Severe cases of hyperkalemia (potassium levels > 6.5 mEq/L) can lead to potentially life-threatening arrhythmias and heart failure.
Hyperkalemia may result from various factors, such as kidney dysfunction, hormonal imbalances, medication side effects, trauma, or excessive potassium intake. Prompt identification and management of hyperkalemia are essential to prevent severe complications and ensure proper treatment.
Fanconi syndrome is a medical condition that affects the proximal tubules of the kidneys. These tubules are responsible for reabsorbing various substances, such as glucose, amino acids, and electrolytes, back into the bloodstream after they have been filtered through the kidneys.
In Fanconi syndrome, there is a defect in the reabsorption process, causing these substances to be lost in the urine instead. This can lead to a variety of symptoms, including:
* Polyuria (excessive urination)
* Polydipsia (excessive thirst)
* Dehydration
* Metabolic acidosis (an imbalance of acid and base in the body)
* Hypokalemia (low potassium levels)
* Hypophosphatemia (low phosphate levels)
* Vitamin D deficiency
* Rickets (softening and weakening of bones in children) or osteomalacia (softening of bones in adults)
Fanconi syndrome can be caused by a variety of underlying conditions, including genetic disorders, kidney diseases, drug toxicity, and heavy metal poisoning. Treatment typically involves addressing the underlying cause, as well as managing symptoms such as electrolyte imbalances and acid-base disturbances.
A transfer RNA (tRNA) molecule that carries the amino acid leucine is referred to as "tRNA-Leu." This specific tRNA molecule recognizes and binds to a codon (a sequence of three nucleotides in mRNA) during protein synthesis or translation. In this case, tRNA-Leu can recognize and pair with any of the following codons: UUA, UUG, CUU, CUC, CUA, and CUG. Once bound to the mRNA at the ribosome, leucine is added to the growing polypeptide chain through the action of aminoacyl-tRNA synthetase enzymes that catalyze the attachment of specific amino acids to their corresponding tRNAs. This ensures the accurate and efficient production of proteins based on genetic information encoded in mRNA.
Acid-sensing ion channels (ASICs) are a type of ion channel protein found in nerve cells (neurons) that are activated by acidic environments. They are composed of homomeric or heteromeric combinations of six different subunits, designated ASIC1a, ASIC1b, ASIC2a, ASIC2b, ASIC3, and ASIC4. These channels play important roles in various physiological processes, including pH homeostasis, nociception (pain perception), and mechanosensation (the ability to sense mechanical stimuli).
ASICs are permeable to both sodium (Na+) and calcium (Ca2+) ions. When the extracellular pH decreases, the channels open, allowing Na+ and Ca2+ ions to flow into the neuron. This influx of cations can depolarize the neuronal membrane, leading to the generation of action potentials and neurotransmitter release.
In the context of pain perception, ASICs are activated by the acidic environment in damaged tissues or ischemic conditions, contributing to the sensation of pain. In addition, some ASIC subunits have been implicated in synaptic plasticity, learning, and memory processes. Dysregulation of ASIC function has been associated with various pathological conditions, including neuropathic pain, ischemia, epilepsy, and neurodegenerative diseases.
In the context of medicine, and specifically in physiology and respiratory therapy, partial pressure (P or p) is a measure of the pressure exerted by an individual gas in a mixture of gases. It's commonly used to describe the concentrations of gases in the body, such as oxygen (PO2), carbon dioxide (PCO2), and nitrogen (PN2).
The partial pressure of a specific gas is calculated as the fraction of that gas in the total mixture multiplied by the total pressure of the mixture. This concept is based on Dalton's law, which states that the total pressure exerted by a mixture of gases is equal to the sum of the pressures exerted by each individual gas.
For example, in room air at sea level, the partial pressure of oxygen (PO2) is approximately 160 mmHg (mm of mercury), which represents about 21% of the total barometric pressure (760 mmHg). This concept is crucial for understanding gas exchange in the lungs and how gases move across membranes, such as from alveoli to blood and vice versa.
Glutaminase is an enzyme that catalyzes the conversion of L-glutamine, which is a type of amino acid, into glutamate and ammonia. This reaction is an essential part of nitrogen metabolism in many organisms, including humans. There are several forms of glutaminase found in different parts of the body, with varying properties and functions.
In humans, there are two major types of glutaminase: mitochondrial and cytosolic. Mitochondrial glutaminase is primarily found in the kidneys and brain, where it plays a crucial role in energy metabolism by converting glutamine into glutamate, which can then be further metabolized to produce ATP (adenosine triphosphate), a major source of cellular energy.
Cytosolic glutaminase, on the other hand, is found in many tissues throughout the body and is involved in various metabolic processes, including nucleotide synthesis and protein degradation.
Glutaminase activity has been implicated in several disease states, including cancer, where some tumors have been shown to have elevated levels of glutaminase expression, allowing them to use glutamine as a major source of energy and growth. Inhibitors of glutaminase are currently being investigated as potential therapeutic agents for the treatment of cancer.
A kidney, in medical terms, is one of two bean-shaped organs located in the lower back region of the body. They are essential for maintaining homeostasis within the body by performing several crucial functions such as:
1. Regulation of water and electrolyte balance: Kidneys help regulate the amount of water and various electrolytes like sodium, potassium, and calcium in the bloodstream to maintain a stable internal environment.
2. Excretion of waste products: They filter waste products from the blood, including urea (a byproduct of protein metabolism), creatinine (a breakdown product of muscle tissue), and other harmful substances that result from normal cellular functions or external sources like medications and toxins.
3. Endocrine function: Kidneys produce several hormones with important roles in the body, such as erythropoietin (stimulates red blood cell production), renin (regulates blood pressure), and calcitriol (activated form of vitamin D that helps regulate calcium homeostasis).
4. pH balance regulation: Kidneys maintain the proper acid-base balance in the body by excreting either hydrogen ions or bicarbonate ions, depending on whether the blood is too acidic or too alkaline.
5. Blood pressure control: The kidneys play a significant role in regulating blood pressure through the renin-angiotensin-aldosterone system (RAAS), which constricts blood vessels and promotes sodium and water retention to increase blood volume and, consequently, blood pressure.
Anatomically, each kidney is approximately 10-12 cm long, 5-7 cm wide, and 3 cm thick, with a weight of about 120-170 grams. They are surrounded by a protective layer of fat and connected to the urinary system through the renal pelvis, ureters, bladder, and urethra.
Dichloroacetic acid (DCA) is a chemical compound with the formula CCl2CO2H. It is a colorless liquid that is used as a reagent in organic synthesis and as a laboratory research tool. DCA is also a byproduct of water chlorination and has been found to occur in low levels in some chlorinated drinking waters.
In the medical field, DCA has been studied for its potential anticancer effects. Preclinical studies have suggested that DCA may be able to selectively kill cancer cells by inhibiting the activity of certain enzymes involved in cell metabolism. However, more research is needed to determine whether DCA is safe and effective as a cancer treatment in humans.
It is important to note that DCA is not currently approved by regulatory agencies such as the U.S. Food and Drug Administration (FDA) for use as a cancer treatment. It should only be used in clinical trials or under the supervision of a qualified healthcare professional.
Nephrocalcinosis is a medical condition characterized by the deposition of calcium salts in the renal parenchyma, specifically within the tubular epithelial cells and interstitium of the kidneys. This process can lead to chronic inflammation, tissue damage, and ultimately impaired renal function if left untreated.
The condition is often associated with metabolic disorders such as hyperparathyroidism, distal renal tubular acidosis, or hyperoxaluria; medications like loop diuretics, corticosteroids, or calcineurin inhibitors; and chronic kidney diseases. The diagnosis of nephrocalcinosis is typically made through imaging studies such as ultrasound, CT scan, or X-ray. Treatment usually involves addressing the underlying cause, modifying dietary habits, and administering medications to control calcium levels in the body.
The rumen is the largest compartment of the stomach in ruminant animals, such as cows, goats, and sheep. It is a specialized fermentation chamber where microbes break down tough plant material into nutrients that the animal can absorb and use for energy and growth. The rumen contains billions of microorganisms, including bacteria, protozoa, and fungi, which help to break down cellulose and other complex carbohydrates in the plant material through fermentation.
The rumen is characterized by its large size, muscular walls, and the presence of a thick mat of partially digested food and microbes called the rumen mat or cud. The animal regurgitates the rumen contents periodically to chew it again, which helps to break down the plant material further and mix it with saliva, creating a more favorable environment for fermentation.
The rumen plays an essential role in the digestion and nutrition of ruminant animals, allowing them to thrive on a diet of low-quality plant material that would be difficult for other animals to digest.
Lactic acidosis
Congenital lactic acidosis
Robert Donald Cohen
Ringer's lactate solution
Tumor lysis syndrome
Exercise intolerance
List of OMIM disorder codes
Adverse effect
Cori cycle
Shock (circulatory)
Lactic acid
High anion gap metabolic acidosis
Multiple organ dysfunction syndrome
Metformin
Positional asphyxia
Glycogen storage disease type VI
Pyruvate dehydrogenase deficiency
Pyruvate dehydrogenase complex
Sodium lactate
MT-TF
Buformin
Strychnine
Glycogen storage disease type 0
Pyruvate carboxylase deficiency
Strychnine poisoning
Hypovolemic shock
Delta ratio
Acidosis
Phosphate carrier protein, mitochondrial
Frank Woods (pharmacologist)
Lactic acidosis - Wikipedia
Lactic Acidosis: Background, Etiology, Epidemiology
Lactic Acidosis: Symptoms, Treatment, Causes, and More
Lactic Acidosis: Causes, Symptoms, and Treatment | HealthNews
Mitochondrial encephalomyopathy lactic acidosis and strokelike episodes mimicking occipital idiopathic epilepsy
Lactic acidosis Information | Mount Sinai - New York
Lactic acidosis
The syndrome of mitochondrial encephalomyopathy, lactic acidosis, and strokelike episodes presenting without stroke
Treatment of congenital lactic acidosis with dichloroacetate | Archives of Disease in Childhood
Ionized calcium in acidosis: differential effect of hypercapnic and lactic acidosis - Zurich Open Repository and Archive
Plasmodium berghei Infection: Dichloroacetate Improves Survival in Rats with Lactic Acidosis - MORU Tropical Health Network
Type B lactic acidosis secondary to thiamine deficiency in a child with malignancy<...
Lactic Acidosis
Lactic acidosis | Diagnosaurus
Metformin lactic acidosis presentation
Severe lactic acidosis reversed by thiamine within 24 hours | Critical Care | Full Text
Lactic acidosis and hypoglycaemia in children with severe malaria: pathophysiological and prognostic significance - Centre for...
Albuterol-Induced Lactic Acidosis | Proceedings
Differential diagnosis of lactic acidosis
Seizure Lactic Acidosis | DiabetesTalk.Net
Nutritional Deficiency Lactic Acidosis Information Videos
What Is Lactic Acidosis | DiabetesTalk.Net
Will stopping metformin reverse lactic acidosis - thesitesale
Lactic Acidosis Treatment You Should Try | Healthcare-Online
Ketoacidosis and Lactic Acidosis - Surprising Top 13 Difference
Acute Lactic Acidosis: Overview, Treatment Overview, Prehospital Care
Phenylbutyrate May Be Repurposed to Treat Lactic Acidosis
Causes of lactic acidosis in sepsis | Deranged Physiology
DailyMed - GLIPIZIDE AND METFORMIN HYDROCHLORIDE tablet, film coated
DailyMed - METFORMIN HYDROCHLORIDE tablet, extended release
Metabolic20
- It is a form of metabolic acidosis, in which excessive acid accumulates due to a problem with the body's oxidative metabolism. (wikipedia.org)
- Symptoms in humans include all those of typical metabolic acidosis (nausea, vomiting, generalized muscle weakness, and laboured and deep breathing). (wikipedia.org)
- With a persistent oxygen debt and overwhelming of the body's buffering abilities (whether from long-term dysfunction or excessive production), hyperlacticaemia and metabolic acidosis ensue, commonly referred to as lactic acidosis. (medscape.com)
- By the turn of the 20th century, many physicians recognized that patients who are critically ill could exhibit metabolic acidosis unaccompanied by elevation of ketones or other measurable anions. (medscape.com)
- Lactic acidosis, on the other hand, is associated with major metabolic dysregulation, tissue hypoperfusion, the effects of certain drugs or toxins, and congenital abnormalities in carbohydrate metabolism. (medscape.com)
- It also occurs as a result on markedly increased transient metabolic demand (eg, postseizure lactic acidosis). (medscape.com)
- Metabolic acidosis. (mountsinai.org)
- 4 mmol/L. It is the most common cause of metabolic acidosis and can be associated with an anion gap metabolic acidosis or mixed acid-base disorder. (logicalimages.com)
- Because of slow metabolism of D-lactic acid, systemic absorption leads to elevated plasma D-lactic acid levels and metabolic acidosis. (logicalimages.com)
- Patients present with episodic metabolic acidosis as well as altered mental status, ataxia, loss of memory, or slurred speech. (logicalimages.com)
- and repeat ABG after 2 hr. to see if acidosis resolved This patient has an acidic pH with a decrease in his bicarbonate concentration suggestive of metabolic acidosis. (diabetestalk.net)
- Metabolic acidosis is defined as a state of decreased systemic pH resulting from either a primary increase in hydrogen ion (H + ) or a reduction in bicarbonate (HCO 3 - ) concentrations. (medscape.com)
- The underlying etiology of metabolic acidosis is classically categorized into those that cause an elevated anion gap (AG) (see the Anion Gap calculator) and those that do not. (medscape.com)
- Lactic acidosis, identified by a state of acidosis and an elevated plasma lactate concentration is one type of anion gap metabolic acidosis and may result from numerous conditions. (medscape.com)
- Ketoacidosis and Lactic Acidosis are two distinct metabolic acidosis conditions. (keydifference.info)
- Yes, ketoacidosis, as well as lactic acidosis, are two distinct medical conditions, even though they both cause metabolic acidosis as well as an unnatural change in blood pH. (keydifference.info)
- Acute or chronic metabolic acidosis, including diabetic ketoacidosis, with or without coma. (nih.gov)
- This condition is distinct from metabolic acidosis, which affects individuals with diabetes. (simple-remedies.com)
- Type B lactic acidosis as a severe metabolic complication in lymphoma and leukemia: a case series from a single institution and literature review. (thieme-connect.de)
- Nonspecific laboratory findings include metabolic and lactic acidosis (1-2). (cdc.gov)
Severe22
- Several decades later, Huckabee's seminal work firmly established that lactic acidosis frequently accompanies severe illnesses and that tissue hypoperfusion underlies the pathogenesis. (medscape.com)
- The most common cause of lactic acidosis is severe medical illness in which blood pressure is low and too little oxygen is reaching the body's tissues. (mountsinai.org)
- If it does not resolve, then look for other potential Choice A, B and C: Use of bicarbonate in the treatment of lactic acidosis is very controversial and is recommended only in severe acute acidosis with pH (diabetestalk.net)
- In severe cases, dialysis may be necessary to remove metformin and lactic acid from the body. (thesitesale.com)
- Dialysis may also be useful when severe lactic acidosis exists in the setting of renal failure or congestive heart failure and, additionally, with severe metformin intoxication. (medscape.com)
- In case of severe lactic acidosis, it is important to take the patient to the hospital without wasting any time. (healthcare-online.org)
- If you're in the hospital for lactic acidosis treatment , your healthcare provider will first consider how severe your symptoms are and if you're also experiencing nausea, vomiting and difficulty breathing. (healthcare-online.org)
- Type A lactic acidosis can be linked to conditions such as severe infections or shock, as well as heart failure. (keydifference.info)
- He was found to have severe lactic acidosis at the time of second relapse. (elsevierpure.com)
- Pharmacokinetics and pharmacodynamics of dichloroacetate in children with lactic acidosis due to severe malaria. (ox.ac.uk)
- Lactic acidosis frequently complicates severe malaria in African children, and is a strong independent predictor of mortality. (ox.ac.uk)
- A single intravenous dose of DCA rapidly improved lactic acidosis in African children with severe malaria, suggesting that DCA may be a useful adjunct in the initial treatment of these patients, and may increase their chance of survival by improving a major complication of their illness. (ox.ac.uk)
- Overall, 2.0% of patients developed moderate to severe symptomatic hyperlactatemia, with 7 (1.0%), all female, diagnosed with lactic acidosis. (researchwithrutgers.com)
- Female gender (P = 0.008) and being overweight, namely having a body mass index (BMI) of greater than 25 (P = 0.001), were predictive for the development of moderate to severe symptomatic hyperlactatemia or lactic acidosis. (researchwithrutgers.com)
- Risk factors for the development of moderate to severe symptomatic hyperlactatemia or lactic acidosis appear to be multifactorial but include female gender and having a BMI of greater than 25. (researchwithrutgers.com)
- Lactic acidosis and severe hepatomegaly with steatosis, including fatal cases, have been reported with the use of nucleoside analogues including RETROVIR. (drugs.com)
- Mold can cause SEVERE symptoms and lactic acid acidosis. (huzzaz.com)
- Severe lactic acidosis may serve as a risk modifier for the SCAI shock classification. (elsevierpure.com)
- Acute decompensation in thiamine-deficient patients may manifest as neurologic or cardiovascular changes, with severe lactic acidosis as the presenting symptom. (thieme-connect.de)
- 1 Svahn J, Schiaffino MC, Caruso U, Calvillo M, Minniti G, Dufour C. Severe lactic acidosis due to thiamine deficiency in a patient with B-cell leukemia/lymphoma on total parenteral nutrition during high-dose methotrexate therapy. (thieme-connect.de)
- Arg82*) in COX16 with hypertrophic cardiomyopathy, encephalopathy and severe fatal lactic acidosis, and isolated complex IV deficiency. (amsterdamumc.org)
- This report describes a case of severe lactic acidosis associated with a suspected succinic semialdehyde dehydrogenase (SSADH) deficiency in a 5-month-old Chihuahua. (huji.ac.il)
Risk of lactic acidosis3
- The older related and now withdrawn drug phenformin carried a much higher risk of lactic acidosis. (wikipedia.org)
- Metformin is known to increase the risk of lactic acidosis, especially in individuals with kidney or liver problems. (thesitesale.com)
- These data indicate that the risk of lactic acidosis with Imeglimin treatment may be lower than with Metformin and confirm that the underlying mechanisms of action are distinct, supporting its potential utility for patients with predisposing conditions. (hal.science)
Buildup of lactic acid5
- Lactic acidosis is a rare but serious condition that occurs when there is an excessive buildup of lactic acid in the blood. (thesitesale.com)
- In some cases, stopping metformin may be necessary to prevent further buildup of lactic acid and improve the patient's condition. (thesitesale.com)
- Lactic acidosis is characterized by the buildup of lactic acid in the blood, leading to a decrease in pH levels and potential organ dysfunction. (thesitesale.com)
- Acidosis means "too much acid in your body", and in lactic acidosis, it refers to the buildup of lactic acid in your bloodstream. (healthcare-online.org)
- Researchers think these drugs can damage mitochondria (your cells' energy factories), leading to a dangerous buildup of lactic acid. (catie.ca)
Diabetic ketoacidosis1
- Experts suggest that lactic acidosis may be associated with diabetic ketoacidosis, which is associated with use of some forms of anti-diabetic drugs like phenformin. (simple-remedies.com)
Case of lactic acidosis2
- In case of lactic acidosis, inadequate supply of oxygen interferes with the cells ability to synthesize ATP to meet its requirements, which results in glycolysis. (simple-remedies.com)
- The CPSolvers share a case of lactic acidosis - let's practice those schemas together! (clinicalproblemsolving.com)
Lead to lactic acidosis3
- When the kidneys are unable to remove metformin from the body efficiently, it can accumulate and lead to lactic acidosis. (thesitesale.com)
- However, in some cases, metformin can lead to lactic acidosis, especially if the drug is not properly monitored or if there are underlying health issues. (thesitesale.com)
- Heavy metal toxicity can also lead to lactic acidosis. (simple-remedies.com)
Types of lactic acidosis1
- Lactic acidosis is caused by elevated levels of lactic acid in the blood due to several factors used to characterize the two types of lactic acidosis: type A and type B. Lactic acidosis type A is a common type resulting from an inadequate supply of oxygen to the blood tissue. (healthnews.com)
Management of lactic acidosis2
- The management of lactic acidosis is targeted toward treating the cause. (healthnews.com)
- During the terminal phase of his disease, he required multiple hospitalizations for management of lactic acidosis and other complications of his MM. No other cause of his elevated lactate levels was identified. (elsevierpure.com)
Suggestive of lactic acidosis2
- post seizure increased anion gap m.acidosis suggestive of lactic acidosis. (diabetestalk.net)
- Suspend treatment if clinical or laboratory findings suggestive of lactic acidosis or pronounced hepatotoxicity occur. (drugs.com)
Development of lactic acidosis2
- The development of lactic acidosis depends on the magnitude of hyperlactatemia, the buffering capacity of the body, and the coexistence of other conditions that produce tachypnea and alkalosis (eg, liver disease, sepsis). (medscape.com)
- Although comorbidities such as liver, kidney, and heart diseases are strongly associated with lactic acidosis, trauma or adverse reaction to medication can also contribute to the development of lactic acidosis. (healthnews.com)
Encephalopathy2
- A third type, D-lactic acidosis (D-lactate encephalopathy) is an unusual form of lactic acidosis. (msdmanuals.com)
- Long-term ketogenic diet therapy improves mitochondrial encephalopathy with lactic acidosis and stroke-like episodes (MELAS): A case report. (bvsalud.org)
Congenital3
- Congenital lactic acidosis is secondary to inborn errors of metabolism, such as defects in gluconeogenesis, pyruvate dehydrogenase, the tricarboxylic acid (TCA) cycle, or the respiratory chain. (medscape.com)
- The term congenital lactic acidosis (CLA) refers to a group of inborn errors of mitochondrial metabolism variably characterised by progressive neuromuscular deterioration and accumulation of lactate and hydrogen ions in blood, urine and/or cerebrospinal fluid, frequently resulting in early death. (bmj.com)
- Other causes of lactic acidosis are rare congenital disorders where mitochondrial don't function adequately. (simple-remedies.com)
Sepsis3
- For example, having lactic acidosis due to sepsis means the doctor will take a targeted approach to managing sepsis. (healthnews.com)
- Type A lactic acidosis - Associated with tissue hypoperfusion caused by circulatory failure from shock, which can be due to many things including sepsis, heart failure, hypovolemia, neurologic compromise, or respiratory failure. (logicalimages.com)
- Incremento de la concentración sanguínea de LACTATO asociada frecuentemente a CHOQUE SÉPTICO, LESIONES PULMONARES, SEPSIS Y TOXICIDAD MEDICAMENTOSA, Cuando la hiperlactatemia se asocia a pH bajo se denomina ACIDOSIS LÁCTICA. (bvsalud.org)
Include lactic acidosis1
- This has been associated with several long-term mitochondrial toxicities, which include lactic acidosis and pancreatitis, peripheral neuropathy, and lipoatrophy. (researchwithrutgers.com)
Profound lactic acidosis2
- We report the case of a 56-year-old man with profound lactic acidosis that resolved rapidly after thiamine infusion. (biomedcentral.com)
- Thiamine is an essential component of cellular metabolism and its deficiency results in potentially life-threatening events and profound lactic acidosis through anaerobic metabolism. (thieme-connect.de)
Liver7
- People who have uncontrolled diabetes, or liver, kidney, or heart diseases are at a higher risk of developing lactic acidosis than those without these comorbidities. (healthnews.com)
- Lactic acidosis can occur due to the liver and kidneys' inability to filter lactic acid from the blood and break it down into glucose, the body's main energy source. (healthnews.com)
- Also, lactic acid filtered by the kidneys and liver is converted into glucose, the body's energy source. (healthnews.com)
- The liver then processes and converts lactic acid into a substance called lactate, which is then cleared from the body. (thesitesale.com)
- Phenylbutyrate also prevented lactic acidosis in mice in which the condition had been induced by removal of part of the liver. (medscape.com)
- The drug may also be helpful to alleviate lactate acidosis in nongenetic conditions, such as asphyxia , liver disease, and ischemia. (medscape.com)
- You need to keep in mind that lactic acidosis will eventually cause certain liver related issues, so it is of immense importance that your doctor keeps a close eye on your liver function while you're using a lactic acidosis treatment. (healthcare-online.org)
Type B lactic8
- Type B lactic acidosis - Due to drug- or toxin-induced impairment of cellular metabolism, ischemia, nutritional deficient state, or rarely malignancy. (logicalimages.com)
- Type B lactic acidosis is an underrecognized clinical entity that must be distinguished from type A (hypoxic) lactic acidosis. (northwestern.edu)
- We briefly review type A versus type B lactic acidosis in this case report. (northwestern.edu)
- Shah, S & Wald, E 2015, ' Type B lactic acidosis secondary to thiamine deficiency in a child with malignancy ', Pediatrics , vol. 135, no. 1, pp. e221-e224. (northwestern.edu)
- This OnePager reviews the physiology of why/how we produce lactic acid and breaks lactic acidosis into two categories: Impaired O2 Delivery (Type A Lactic Acidosis) and Impaired O2 clearance/utilization (Type B Lactic Acidosis). (tactuum.com)
- Type B lactic acidosis occurs in states of normal global tissue perfusion (and hence ATP production) and is less ominous. (msdmanuals.com)
- Type B lactic acidosis is rare among patients with malignant diseases. (elsevierpure.com)
- Although type B lactic acidosis may more commonly occur in patients with leukemia or lymphoma, it may rarely present in patients with rapidly progressive and refractory MM. (elsevierpure.com)
Accumulation of lactic acid2
- In 1925, Clausen identified the accumulation of lactic acid in blood as a cause of acid-base disorder. (medscape.com)
- Since metformin is the underlying cause of lactic acidosis in these cases, discontinuing the medication is necessary to prevent further accumulation of lactic acid. (thesitesale.com)
Metformin32
- Some drugs, including metformin , a drug used to treat diabetes , and all nucleoside reverse transcriptase inhibitor (NRTI) drugs used to treat HIV /AIDS can cause lactic acidosis. (webmd.com)
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- Some medical conditions can also bring on lactic acidosis, including: Vitamin B deficiency Shock Some drugs, including metformin, a drug used to treat diabetes, and all nucleoside reverse transcriptase inhibitor (NRTI) drugs used to treat HIV/AIDS can cause lactic acidosis. (diabetestalk.net)
- Learn about the potential effects of stopping metformin on lactic acidosis, a rare but serious side effect of this medication. (thesitesale.com)
- Find out if discontinuing metformin can help reverse lactic acidosis and what steps should be taken if you suspect this condition. (thesitesale.com)
- In cases of metformin-induced lactic acidosis, it is important to determine whether stopping the medication can reverse the condition. (thesitesale.com)
- Metformin-induced lactic acidosis is a potentially life-threatening condition that requires immediate medical attention. (thesitesale.com)
- Therefore, it is crucial to seek medical help if you suspect you may be experiencing lactic acidosis while taking metformin. (thesitesale.com)
- While stopping metformin may help in some cases of lactic acidosis, it is not a guaranteed solution. (thesitesale.com)
- Metformin and Lactic Acidosis: Can Stopping the Medication Reverse the Condition? (thesitesale.com)
- Lactic acidosis is a rare but potentially life-threatening complication that can occur as a side effect of metformin, a medication commonly used to treat type 2 diabetes. (thesitesale.com)
- It is essential to understand the relationship between metformin and lactic acidosis to determine whether stopping the medication can reverse the condition. (thesitesale.com)
- While it is generally well-tolerated, there have been rare cases where metformin can cause lactic acidosis, especially in individuals with impaired kidney function. (thesitesale.com)
- Stopping metformin is a crucial step in managing lactic acidosis associated with the medication. (thesitesale.com)
- It could be a rare side effect of certain medications, such as metformin and HIV drugs in the NRTI or nucleoside reverse transcriptase inhibitor, hindering the breakdown of lactic acid and causing lactic acidosis. (healthcare-online.org)
- Postmarketing cases of metformin-associated lactic acidosis have resulted in death, hypothermia, hypotension, and resistant bradyarrhythmias. (nih.gov)
- Steps to reduce the risk of and manage metformin-associated lactic acidosis in these high risk groups are provided in the Full Prescribing Information. (nih.gov)
- If lactic acidosis is suspected, discontinue metformin hydrochloride extended-release tablets and institute general supportive measures in a hospital setting. (nih.gov)
- Contrary to clinical belief, metformin doesn't cause lactic acidosis, though clinicians doubt this claim. (simple-remedies.com)
- Metformin is a widely used biguanide T2D therapy, associated with rare but serious events of lactic acidosis, in particular with predisposing conditions (e.g., renal failure or major surgery). (hal.science)
- In a dog model of major surgery, Metformin or Imeglimin (30-1000 mg/kg) was acutely administered, only Metformin-induced lactate accumulation and pH decrease leading to lactic acidosis with fatality at the highest dose. (hal.science)
Hyperlactatemia2
- Thus, hyperlactatemia or lactic acidosis may be associated with acidemia, a normal pH, or alkalemia. (medscape.com)
- When hyperlactatemia is associated with low body pH (acidosis) it is LACTIC ACIDOSIS. (bvsalud.org)
Produce lactic acid1
- Cells produce lactic acid to generate additional energy in the absence of oxygen during intense physical activity. (healthnews.com)
Body's2
Acute3
- Lactic acidosis is typically the result of an underlying acute or chronic medical condition, medication, or poisoning. (wikipedia.org)
- Go to Acute Lactic Acidosis for complete information on this topic. (medscape.com)
- In the acute state, respiratory compensation of acidosis occurs by hyperventilation resulting in a relative reduction in PaCO 2 . (medscape.com)
Abdominal pain2
- The symptoms of lactic acidosis can vary, but may include weakness, fatigue, shortness of breath, and abdominal pain. (thesitesale.com)
- Signs of lactic acidosis could consist of muscle weakness fast breathing, abdominal pain nausea, as well as an altered state of mind. (keydifference.info)
Bloodstream8
- Lactic acidosis is a medical condition characterized by a build-up of lactate (especially L-lactate) in the body, with formation of an excessively low pH in the bloodstream. (wikipedia.org)
- But this lactate or lactic acid can build up in your bloodstream faster than you can burn it off. (webmd.com)
- It is characterized by excessive amounts of lactic acid in the bloodstream due to oxygen deprivation. (healthnews.com)
- Lactic acidosis is a medical condition driven by heightened levels of lactic acid in the bloodstream caused by an inadequate supply of oxygen to the body tissue or an altered metabolism mediated by drugs or toxins. (healthnews.com)
- Lactic acidosis refers to lactic acid build up in the bloodstream. (mountsinai.org)
- Lactic acidosis is a medical condition characterized by the buildup of lactate (especially L-lactate) in the body, which results in an excessively low pH in the bloodstream. (diabetestalk.net)
- Lactic acidosis occurs when the body produces too much lactic acid or cannot effectively remove it from the bloodstream. (thesitesale.com)
- Lactic Acidosis can be described as a health disorder characterized by the build-up of lactic acid within the bloodstream. (keydifference.info)
Toxicity2
- Clinicians believe that mitochondrial toxicity caused by the long term use of the drug can trigger lactic acidosis. (simple-remedies.com)
- Those diagnosed with lactic acidosis had a mean BMI of 32.38 (interquartile range [IQR] = 29.4 to 35) at the time of toxicity and had been receiving HAART for a mean of 12.1 months (IQR = 7 to 20.8). (researchwithrutgers.com)
Excess lactic acid2
- Treatment may involve intravenous fluids to hydrate the body and improve blood flow, as well as medications to help remove excess lactic acid from the blood. (thesitesale.com)
- Lactic acidosis is a medical condition caused mainly due to the excess lactic acid in your blood. (healthcare-online.org)
Dichloroacetate1
- In rare chronic forms of lactic acidosis caused by mitochondrial disease, a specific diet or dichloroacetate may be used. (wikipedia.org)
Nucleoside1
- Although other medications can cause lactic acidosis, most cases have occurred in people using nucleoside analogues (nukes). (catie.ca)
Diagnosis1
- The diagnosis is made on biochemical analysis of blood (often initially on arterial blood gas samples), and once confirmed, generally prompts an investigation to establish the underlying cause to treat the acidosis. (wikipedia.org)
Deficiency2
- Thiamine deficiency is an underdiagnosed cause of lactic acidosis, although treatment is safe, inexpensive, and readily available. (biomedcentral.com)
- Some suggest that lactic acidosis can also result from the deficiency of vitamin B1 or thiamine. (simple-remedies.com)
Metabolism7
- The human metabolism produces about 20 mmol/kg of lactic acid every 24 hours. (wikipedia.org)
- In "type A" lactic acidosis, the production of lactate is attributable to insufficient oxygen for aerobic metabolism. (wikipedia.org)
- In basic terms, lactic acid is essentially a carbohydrate within cellular metabolism and its levels rise with increased metabolism during exercise and with catecholamine stimulation. (medscape.com)
- On the other hand, lactic acidosis type B is a rare type resulting from altered metabolism by drugs or toxins. (healthnews.com)
- Lactic acid is produced when oxygen levels become low in cells within the areas of the body where metabolism takes place or in response to sympathetic overactivity related to epinephrine-type substances or exercise. (mountsinai.org)
- Lactic acidosis results from overproduction of lactate, decreased metabolism of lactate, or both. (msdmanuals.com)
- D-lactic acid is normally produced in small quantities as the product of carbohydrate metabolism by bacteria in the colon. (msdmanuals.com)
Left untreated2
- If left untreated, lactic acidosis can lead to organ damage and even death. (thesitesale.com)
- Lactic acidosis can be fatal if left untreated. (justicecounts.com)
Encephalomyopathy4
- The eventual development of status epilepticus, associated with a T(1) hypointense as well as T(2), fluid-attenuated inversion recovery, and diffusion-weighted hyperintense brain lesion led to pathologic and genetic testing that identified a A3243G mitochondrial DNA point mutation associated with mitochondrial, encephalomyopathy, lactic acidosis, and strokelike episodes. (nih.gov)
- This case emphasizes that occipital epileptic seizures can be the only presenting and long-lasting sign in patients with mitochondrial, encephalomyopathy, lactic acidosis, and strokelike episodes. (nih.gov)
- To study and describe a large family with the tRNA Leu(UUR) point mutation at position 3243 in mitochondrial DNA, which is associated with the syndrome of mitochondrial encephalomyopathy, lactic acidosis, and strokelike episodes. (nih.gov)
- Clinical evaluation, muscle biopsy, and mitochondrial DNA point mutation quantitation of the syndrome of mitochondrial encephalomyopathy, lactic acidosis, and strokelike episodes in muscle and blood. (nih.gov)
Treatment13
- Lactic acid treatment reduces the production of pro-inflammatories and increases the production of anti-inflammatories in the body. (healthnews.com)
- this caused by accelerated production of lactic acid in muscle and reduced hepatic lactate uptake however this post ictal lactic acidosis is transeint and resloves without treatment within 60 to 90 min so best intervention is to observe with 60 to 90 min. (diabetestalk.net)
- However, this post-ictal lactic acidosis is transient and resolves without treatment within 60 to 90 minutes. (diabetestalk.net)
- If lactic acidosis is suspected, individuals should seek medical help promptly to receive appropriate treatment. (thesitesale.com)
- Initial treatment of lactic acidosis predicates an understanding of basic resuscitation and the ability to have testing modalities present to identify the elevation. (medscape.com)
- The treatment may have wider applications, because lactic acidosis is a secondary effect of other pathologies. (medscape.com)
- It is important to identify the exact cause to find the right treatment for lactic acidosis. (healthcare-online.org)
- You need to inform your healthcare provider of your symptoms so they could select the best treatment of lactic acidosis. (healthcare-online.org)
- The doctor will select a proper treatment of lactic acidosis to stabilize the patient's condition. (healthcare-online.org)
- If you're a patient of lactic acidosis and are looking for a suitable lactic acidosis treatment, you should pay attention to the following things first. (healthcare-online.org)
- What lactic acidosis treatment is right for you usually depends on your lactate value. (healthcare-online.org)
- They will also explain when you can start them again and which ones you have to take when you start the lactic acidosis treatment again. (healthcare-online.org)
- It is usually important to change your HIV treatment regimen if your lactate levels are low and you don't have any lactic acidosis symptoms. (healthcare-online.org)
Occurs when the body produces1
- However, it typically occurs when the body produces excessive amounts of lactic acid, than desired. (healthnews.com)
Ketoacidosis1
- Is ketoacidosis different from lactic acidosis? (keydifference.info)
Typically2
- Lactic acidosis typically occurs when lactic acid production exceeds clearance, often in the setting of impaired tissue oxygenation and defective mitochondrial oxygenation. (logicalimages.com)
- Once lactic acidosis has developed, medical intervention is typically required to correct the acid-base imbalance and support organ function. (thesitesale.com)
Commonly2
- Numerous etiologies may be responsible for the presence of lactic acidosis, most commonly circulatory failure and hypoxia. (medscape.com)
- Lactic acidosis is commonly seen in people over 40. (healthnews.com)