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
Carbon monoxide poisoning treated with hyperbaric oxygen: metabolic acidosis as a predictor of treatment requirements. (1/136)
A retrospective case note analysis was made of patients who received hyperbaric oxygen for carbon monoxide poisoning and were admitted to the Royal Naval Hospital Haslar between 1991 and 1995. Males predominated (38 v 10) as did cases of deliberate self poisoning (31 v 17). The most common presenting feature was unconsciousness, which is an indication for hyperbaric oxygen and therefore reflects referral patterns. If patients had not recovered completely after one hyperbaric exposure further treatments were given. The initial hydrogen ion concentration of those requiring more than one treatment was significantly higher than those who recovered after the first treatment. The initial carboxyhaemoglobin (COHb) concentration showed only a trend to being higher in the multiple treatment group. Although metabolic acidosis is well recognised, its relationship to treatment requirements has not been shown previously. Initial COHb does not always correlate well with severity of poisoning which relates to the mechanism of toxicity of carbon monoxide: binding of carbon monoxide to the intracellular oxygen carrying proteins (for example cytochromes) rather than solely to haemoglobin. These findings are consistent with this mechanism and suggests that initial acidosis is a better predictor of treatment requirements and severity than initial COHb. (+info)Renal responses of trout to chronic respiratory and metabolic acidoses and metabolic alkalosis. (2/136)
Exposure to hyperoxia (500-600 torr) or low pH (4.5) for 72 h or NaHCO(3) infusion for 48 h were used to create chronic respiratory (RA) or metabolic acidosis (MA) or metabolic alkalosis in freshwater rainbow trout. During alkalosis, urine pH increased, and [titratable acidity (TA) - HCO(-)(3)] and net H(+) excretion became negative (net base excretion) with unchanged NH(+)(4) efflux. During RA, urine pH did not change, but net H(+) excretion increased as a result of a modest rise in NH(+)(4) and substantial elevation in [TA - HCO(-)(3)] efflux accompanied by a large increase in inorganic phosphate excretion. However, during MA, urine pH fell, and net H(+) excretion was 3.3-fold greater than during RA, reflecting a similar increase in [TA - HCO(-)(3)] and a smaller elevation in phosphate but a sevenfold greater increase in NH(+)(4) efflux. In urine samples of the same pH, [TA - HCO(-)(3)] was greater during RA (reflecting phosphate secretion), and [NH(+)(4)] was greater during MA (reflecting renal ammoniagenesis). Renal activities of potential ammoniagenic enzymes (phosphate-dependent glutaminase, glutamate dehydrogenase, alpha-ketoglutarate dehydrogenase, alanine aminotransferase, phosphoenolpyruvate carboxykinase) and plasma levels of cortisol, phosphate, ammonia, and most amino acids (including glutamine and alanine) increased during MA but not during RA, when only alanine aminotransferase increased. The differential responses to RA vs. MA parallel those in mammals; in fish they may be keyed to activation of phosphate secretion by RA and cortisol mobilization by MA. (+info)In vitro metabolic and respiratory acidosis selectively inhibit osteoblastic matrix gene expression. (3/136)
Clinically, a decrease in blood pH may be due to either a reduction in bicarbonate concentration ([HCO(-)(3)], metabolic acidosis) or an increase in PCO(2) (respiratory acidosis). In mammals, metabolic acidosis induces a far greater increase in urine calcium excretion than respiratory acidosis. In cultured bone, metabolic acidosis induces a marked increase in calcium efflux and a decrease in osteoblastic collagen synthesis, whereas isohydric respiratory acidosis has little effect on either parameter. We have shown that metabolic acidosis prevents the normal developmental increase in the expression of RNA for matrix Gla protein and osteopontin in chronic cultures of primary murine calvarial bone cells (predominantly osteoblasts) but does not alter expression of osteonectin. To compare the effects of isohydric metabolic and respiratory acidosis on expression of these genes, bone cell cultures were incubated in medium at pH approximately 7.2 to model metabolic ([HCO(-)(3)], approximately 13 mM) or respiratory (PCO(2), approximately 80 mmHg) acidosis or at pH approximately 7.4 as a control. Cells were sampled at weeks 4, 5, and 6 to assess specific RNA content. At all time periods studied, both metabolic and respiratory acidosis inhibited the expression of RNA for matrix Gla protein and osteopontin to a similar extent, whereas there was no change in osteonectin expression. In contrast to the significant difference in the effects of metabolic and respiratory acidosis on bone calcium efflux and osteoblastic collagen synthesis, these two forms of acidosis have a similar effect on osteoblastic RNA expression of both matrix Gla protein and osteopontin. Thus, although several aspects of bone cell function are dependent on the type of acidosis, expression of these two matrix genes appears to be regulated by extracellular pH, independently of the type of acidosis. (+info)Oxygen therapy during exacerbations of chronic obstructive pulmonary disease. (4/136)
Venturi masks (VMs) and nasal prongs (NPs) are widely used to treat acute respiratory failure (ARF) in chronic obstructive pulmonary disease (COPD). In this study, these devices were compared in terms of their potentiality to worsen respiratory acidosis and their capacity to maintain adequate (> 90%) arterial oxygenation (Sa,O2) through time (approximately 24 h). In a randomized cross-over study, 18 consecutive COPD patients who required hospitalization because of ARF were studied. After determining baseline arterial blood gas levels (on room air), patients were randomized to receive oxygen therapy through a VM or NPs at the lowest possible inspiratory oxygen fraction that resulted in an initial Sa,O2 of > or = 90%. Arterial blood gas levels were measured again 30 min later (on O2), and Sa,O2 recorded using a computer during the subsequent approximately 24 h. Patients were then crossed-over to receive O2 therapy by means of the alternative device (NPs or VM), and the same measurements obtained again in the same order. It was observed that both the VM and NPs improved arterial oxygen tension (p<0.0001) to the same extent (p=NS), without any significant effect upon arterial carbon dioxide tension or pH. However, despite this adequate initial oxygenation, Sa,O2 was < 90% for 3.7+/-3.8 h using the VM and for 5.4+/-5.9 h using NPs (p<0.05). Regression analysis showed that the degree of arterial hypoxaemia (p<0.05) and arterial hypercapnia (p<0.05) present before starting O2 therapy and, particularly, the initial Sa,O2 achieved after initiation of O2 therapy (p<0.0001) enabled the time (in h) that patients would be poorly oxygenated (Sa,O2 < 90%) on follow-up to be predicted. These findings suggest that, in order to maintain an adequate (> 90%) level of arterial oxygenation in patients with chronic obstructive pulmonary disease and moderate acute respiratory failure: 1) the initial arterial oxygen saturation on oxygen should be maximized whenever possible by increasing the inspiratory oxygen fraction; 2) this strategy seems feasible because neither the VM nor NPs worsen respiratory acidosis significantly; and 3) the Venturi mask (better than nasal prongs) should be recommended. (+info)Inspiratory pressure support prolongs exercise induced lactataemia in severe COPD. (5/136)
BACKGROUND: A physiological benefit from pulmonary rehabilitation in chronic obstructive pulmonary disease (COPD) is more probable if exercise is performed above the lactate threshold. This study was undertaken to investigate whether it was possible to extend the lactataemia of exercise using non-invasive inspiratory pressure support (IPS). METHODS: Plasma lactate levels were measured in eight men with severe COPD who performed two treadmill walks at an identical constant work rate to a condition of severe dyspnoea; the second walk was supported by IPS. RESULTS: Mean plasma lactate levels before the free and IPS assisted walks were 1.65 mmol/l and 1. 53 mmol/l, respectively (p = NS). Lactate levels increased during both walks to 2.96 mmol/l and 2.42 mmol/l, respectively (p = 0.01 for each) but the duration of the IPS assisted walk was significantly greater than the free walk (13.6 minutes versus 5.5 minutes, p = 0.01). CONCLUSIONS: Patients with severe COPD can sustain exercise induced lactataemia for longer if assisted with IPS. This technique may prove to be a useful adjunct in pulmonary rehabilitation. (+info)One year period prevalence study of respiratory acidosis in acute exacerbations of COPD: implications for the provision of non-invasive ventilation and oxygen administration. (6/136)
BACKGROUND: Non-invasive ventilation (NIV) reduces mortality and intubation rates in patients with chronic obstructive pulmonary disease (COPD) admitted to hospital with respiratory acidosis. This study aimed to determine the prevalence of respiratory acidosis in patients admitted with COPD, to draw inferences about oxygen therapy, and to determine the need for NIV services for acute COPD in typical UK hospitals. METHODS: This one year prospective prevalence study identified patients with COPD aged 45-79 years inclusive who were admitted to Leeds General Infirmary, St James's University, and Killingbeck Hospitals, Leeds between 1 March 1997 and 28 February 1998. The prevalence of respiratory acidosis and the relationship with oxygenation are described. Other outcomes included intensive care use and in hospital mortality. From this data population prevalence estimates were determined for respiratory acidosis, from which the need for NIV in a typical district general hospital was modelled. RESULTS: 983 patients were admitted, 11 of whom required immediate intubation. 20% of the remaining 972 had a respiratory acidosis. Acidosis was associated with subsequent admission to the intensive care unit (ICU): pH<7.25, OR 6.10 (95% confidence interval (CI) 1.19 to 31.11); pH 7.25-7.30, OR 8.73 (95% CI 2.11 to 36.06). pH was inversely correlated with arterial oxygen tension (PaO(2)) in the 47% of patients who were hypercapnic, with a PaO(2) of >10 kPa being associated with acidosis in most hypercapnic patients. 80% remained acidotic after initial treatment, giving an age/sex specific prevalence for England and Wales of 75 (95% CI 61 to 90)/100 000/year for men aged 45-79 years and 57 (95% CI 46 to 69)/100 000/year for women. Modelling the need for NIV for all COPD patients indicates that a typical UK hospital will admit 90 patients per year with acidosis of which 72 will require NIV. CONCLUSIONS: In patients with acute COPD the PaO(2) should be maintained at 7.3-10 kPa (SaO(2) 85-92%) to avoid the dangers of hypoxia and acidosis. If all COPD patients with a respiratory acidosis (pH<7.35) after initial treatment are offered NIV, a typical UK hospital will treat 72 patients per year. (+info)Cardiovascular responses to calcium administered intravenously to man during halothane anesthesia. (7/136)
Calcium chloride (7 mg/kg) was administered intravenously to six healthy volunteers anesthetized with halothane. Cardiovascular changes were measured during constant ventilation and anesthetic depth under three conditions: 1) respiratory alkalosis, 2) normocarbia, and 3) respiratory acidosis. At each Paco2, calcium infusion significantly increased cardiac index, left ventricular minute work index, and stroke index. Heart rate, total peripheral resistance, and cardiac pre-ejection period decreased. No significant change in mean arterial blood pressure or central venous pressure followed calcium administration, and no arrhythmias occurred. It is concluded that calcium administration increases myocardial performance, presumably by increasing the availability of intracellular calcium ion for actomyosin interaction. (+info)Fumonisin B(1) increases serum sphinganine concentration but does not alter serum sphingosine concentration or induce cardiovascular changes in milk-fed calves. (8/136)
Fumonisin B(1) is the most toxic and commonly occurring form of a group of mycotoxins that alter sphingolipid biosynthesis and induce leukoencephalomalacia in horses and pulmonary edema in pigs. Purified fumonisin B(1) (1 mg/kg, iv, daily) increased serum sphinganine and sphingosine concentrations and decreased cardiovascular function in pigs within 5 days. We therefore examined whether the same dosage schedule of fumonisin B(1) produced a similar effect in calves. Ten milk-fed male Holstein calves were instrumented to obtain blood and cardiovascular measurements. Treated calves (n = 5) were administered purified fumonisin B(1) at 1 mg/kg, iv, daily for 7 days and controls (n = 5) were administered 10 ml 0.9% NaCl, iv, daily. Each calf was euthanized on day 7. In treated calves, serum sphinganine concentration increased from day 3 onward (day 7, 0.237 +/- 0.388 micromol/l; baseline, 0.010 +/- 0.007 micromol/l; mean +/- SD), whereas, serum sphingosine concentration was unchanged (day 7, 0.044 +/- 0.065 micromol/l; baseline, 0.021 +/- 0.025 micromol/l). Heart rate, cardiac output, stroke volume, mean arterial pressure, mean pulmonary artery pressure, pulmonary artery wedge pressure, central venous pressure, plasma volume, base-apex electrocardiogram, arterial Po(2), and systemic oxygen delivery were unchanged in treated and control calves. Fumonisin-treated calves developed metabolic acidosis (arterial blood pH, 7.27 +/- 0.11; base excess, -9.1 +/- 7.6 mEq/l), but all survived for 7 days. We conclude that calves are more resistant to fumonisin B(1) cardiovascular toxicity than pigs. (+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.