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
Kidney
Dichloroacetic Acid
Nephrocalcinosis
Rumen
Metabolic acidosis-induced retinopathy in the neonatal rat. (1/1411)
PURPOSE: Carbon dioxide (CO2)-induced retinopathy (CDIR) in the neonatal rat, analogous to human retinopathy of prematurity (ROP), was previously described by our group. In this model, it is possible that CO2-associated acidosis provides a biochemical mechanism for CDIR. Therefore, the effect of pure metabolic acidosis on the developing retinal vasculature of the neonatal rat was investigated. METHODS: A preliminary study of arterial blood pH was performed to confirm acidosis in our model. In neonatal rats with preplaced left carotid artery catheters, acute blood gas samples were taken 1 to 24 hours after gavage with either NH4Cl 1 millimole/100 g body weight or saline. In the subsequent formal retinopathy study, 150 newborn Sprague-Dawley rats were raised in litters of 25 and randomly assigned to be gavaged twice daily with either NH4Cl 1 millimole/100 g body weight (n = 75) or saline (n = 75) from day 2 to day 7. After 5 days of recovery, rats were killed, and retinal vasculature was assessed using fluorescein perfusion and ADPase staining techniques. RESULTS: In the preliminary pH study, the minimum pH after NH4Cl gavage was 7.10+/-0.10 at 3 hours (versus 7.37+/-0.03 in controls, mean +/- SD, P < 0.01). In the formal retinopathy study, preretinal neovascularization occurred in 36% of acidotic rats versus 5% of controls (P < 0.001). Acidotic rats showed growth retardation (final weight 16.5+/-3.0 g versus 20.2+/-2.6 g, P < 0.001). The ratio of vascularized to total retinal area was smaller in acidotic rats (94%+/-4% versus 96%+/-2%, P < 0.001). CONCLUSIONS: Metabolic acidosis alone induces neovascularization similar to ROP in the neonatal rat. This suggests a possible biochemical mechanism by which high levels of CO2 induce neovascularization and supports the suggestion that acidosis may be an independent risk factor for ROP. (+info)Arteriovenous differences for amino acids and lactate across kidneys of normal and acidotic rats. (2/1411)
1. Arteriovenous differences fro amino acids across kidneys of normal and chronically acidotic rats were measured. Glutamine was the only amino acid extracted in increased amounts in acidosis. There was a considerable production of serine by kidneys from both normal and acidotic rats. 2. The arterial blood concentration of glutamine was significantly decreased in acidotic animals. 3. The glutamine extracted by kidneys of acidotic rats was largely and probably exclusively derived from the plasma. 4. The blood lactate concentration was unchanged in acidosis, as was the uptake of lactate by the kidney. (+info)Abnormal ductus venosus blood flow: a clue to umbilical cord complication. (3/1411)
We report a case of umbilical cord complication causing, fetal hypoxemia and acidemia. At 30 weeks of gestation, the patient was referred because of slightly increased amniotic fluid volume and a non-reactive cardiotocogram. Biometry was appropriate for gestational age. Umbilical artery and fetal aortic Doppler findings were normal, whereas diastolic blood flow velocities in the middle cerebral artery were increased and the ductus venosus showed severely abnormal flow velocity waveforms with reversal of flow during atrial contraction. Since other reasons for fetal hypoxemia could be excluded, careful examination of the umbilical cord was performed. Traction of the hypercoiled umbilical cord due to its course around the fetal neck and shoulders was suspected. Cesarean section confirmed the sonographic findings and fetal blood gases revealed fetal acidemia. This case indicates that investigation of fetal venous blood flow may also help to identify fetal jeopardy due to reasons other than increased placental vascular resistance. (+info)Epidural analgesia with bupivacaine does not improve splanchnic tissue perfusion after aortic reconstruction surgery. (4/1411)
Inadequate splanchnic tissue perfusion is relatively common during and after aortic surgery. We hypothesized that vasodilation caused by thoracic epidural analgesia improves splanchnic blood flow and tissue perfusion after aortic surgery. In this prospective, randomized, controlled study, we studied 20 patients undergoing elective aortic-femoral or aortic-iliac reconstruction surgery. Gastric and sigmoid colon mucosal PCO2 and pH were measured during surgery. An epidural bolus of bupivacaine 40 mg followed by infusion of 15 mg h-1 was started after operation in 10 patients. After operation, splanchnic blood flow and gastric and sigmoid colon mucosal PCO2 and pH were measured before and 2 h after the start of epidural analgesia. During surgery, the gastric mucosal-arterial PCO2 difference remained stable, whereas the sigmoid mucosal-arterial PCO2 difference increased during aortic clamping but returned to pre-clamping values after declamping. After operation, epidural analgesia had no effect on gastric or sigmoid mucosal-arterial PCO2 differences or on splanchnic blood flow. (+info)Temporal differences in actions of calcium channel blockers on K+ accumulation, cardiac function, and high-energy phosphate levels in ischemic guinea pig hearts. (5/1411)
We investigated temporal differences in the protective action of three types of Ca2+ channel blockers in myocardial ischemia, focusing particularly on the blocking ability under depolarizing conditions. The effects of diltiazem, verapamil, and nifedipine on extracellular potassium concentration ([K+]e), acidosis, and level of metabolic markers were examined during 30-min global ischemia and postischemic left ventricular (LV) function in isolated guinea pig hearts. Diltiazem and verapamil, but not nifedipine, inhibited the late phase (15-30 min) of [K+]e elevation, whereas all three blockers delayed the onset of the early phase (0-8 min) of [K+]e elevation. Diltiazem and verapamil inhibited ischemic contracture and improved postischemic LV function to a greater extent. These differences appeared to be linked to preservation of ATP and creatine phosphate and delay of cessation of anaerobic glycolytic activity. Maneuvers to preserve energy sources during ischemia (decrease in external Ca2+ concentration or pacing at a lower frequency) attenuated the late phase of [K+]e elevation. Inhibition of LV pressure was potentiated 12- and 8.2-fold by diltiazem and verapamil, respectively, at 8.9 mM K+ as compared with 2.9 mM K+, whereas that by nifedipine was unchanged. These results indicate that the differential cardioprotection of Ca2+ channel blockers in the late period of ischemia correlates with preservation of high-energy phosphates as a result of different Ca2+ channel blocking abilities under high [K+]e conditions. (+info)Rapid saline infusion produces hyperchloremic acidosis in patients undergoing gynecologic surgery. (6/1411)
BACKGROUND: Changes in acid-base balance caused by infusion of a 0.9% saline solution during anesthesia and surgery are poorly characterized. Therefore, the authors evaluated these phenomena in a dose-response study. METHODS: Two groups of 12 patients each who were undergoing major intraabdominal gynecologic surgery were assigned randomly to receive 0.9% saline or lactated Ringer's solution in a dosage of 30 ml x kg(-1) x h(-1). The pH, arterial carbon dioxide tension, and serum concentrations of sodium, potassium, chloride, lactate, and total protein were measured in 30-min intervals. The serum bicarbonate concentration was calculated using the Henderson-Hasselbalch equation and also using the Stewart approach from the strong ion difference and the amount of weak plasma acid. The strong ion difference was calculated as serum sodium + serum potassium - serum chloride - serum lactate. The amount of weak plasma acid was calculated as the serum total protein concentration in g/dl x 2.43. RESULTS: Infusion of 0.9% saline, but not lactated Ringer's solution, caused a metabolic acidosis with hyperchloremia and a concomitant decrease in the strong ion difference. Calculating the serum bicarbonate concentration using the Henderson-Hasselbalch equation or the Stewart approach produced equivalent results. CONCLUSIONS: Infusion of approximately 30 ml x kg(-1) x h(-1) saline during anesthesia and surgery inevitably leads to metabolic acidosis, which is not observed after administration of lactated Ringer's solution. The acidosis is associated with hyperchloremia. (+info)Evaluation of signals activating ubiquitin-proteasome proteolysis in a model of muscle wasting. (7/1411)
The ubiquitin-proteasome proteolytic system is stimulated in conditions causing muscle atrophy. Signals initiating this response in these conditions are unknown, although glucocorticoids are required but insufficient to stimulate muscle proteolysis in starvation, acidosis, and sepsis. To identify signals that activate this system, we studied acutely diabetic rats that had metabolic acidosis and increased corticosterone production. Protein degradation was increased 52% (P < 0.05), and mRNA levels encoding ubiquitin-proteasome system components, including the ubiquitin-conjugating enzyme E214k, were higher (transcription of the ubiquitin and proteasome subunit C3 genes in muscle was increased by nuclear run-off assay). In diabetic rats, prevention of acidemia by oral NaHCO3 did not eliminate muscle proteolysis. Adrenalectomy blocked accelerated proteolysis and the rise in pathway mRNAs; both responses were restored by administration of a physiological dose of glucocorticoids to adrenalectomized, diabetic rats. Finally, treating diabetic rats with insulin for >/=24 h reversed muscle proteolysis and returned pathway mRNAs to control levels. Thus acidification is not necessary for these responses, but glucocorticoids and a low insulin level in tandem activate the ubiquitin-proteasome proteolytic system. (+info)Changes in intracellular Na+ and pH in rat heart during ischemia: role of Na+/H+ exchanger. (8/1411)
The role of the Na+/H+ exchanger in rat hearts during ischemia and reperfusion was investigated by measurements of intracellular Na+ concentration ([Na+]i) and intracellular and extracellular pH. Under our standard conditions (2-Hz stimulation), 10 min of ischemia caused no significant rise in [Na+]i but an acidosis of 1.0 pH unit, suggesting that the Na+/H+ exchanger was inactive during ischemia. This was confirmed by showing that the Na+/H+ exchange inhibitor methylisobutyl amiloride (MIA) had no effect on [Na+]i or on intracellular pH during ischemia. However, there was a short-lived increase in [Na+]i of 8.2 +/- 0.6 mM on reperfusion, which was reduced by MIA, showing that the Na+/H+ exchanger became active on reperfusion. To investigate the role of metabolic changes, we measured [Na+]i during anoxia. The [Na+]i did not change during 10 min of anoxia, but there was a small, transient rise of [Na+]i on reoxygenation, which was inhibited by MIA. In addition, we show that the Na+/H+ exchanger, tested by sodium lactate exposure, was inhibited during anoxia. These results show that the Na+/H+ exchanger is inhibited during ischemia and anoxia, probably by an intracellular metabolic mechanism. The exchanger activates rapidly on reperfusion and can cause a rapid rise in [Na+]i. (+info)There are several types of acidosis, including:
1. Respiratory acidosis: This occurs when the lung's ability to remove carbon dioxide from the blood is impaired, leading to an increase in blood acidity.
2. Metabolic acidosis: This type of acidosis occurs when there is an excessive production of acid in the body due to factors such as diabetes, starvation, or kidney disease.
3. Mixed acidosis: This type of acidosis is a combination of respiratory and metabolic acidosis.
4. Severe acute respiratory acidosis (SARA): This is a life-threatening condition that occurs suddenly, usually due to a severe lung injury or aspiration of a corrosive substance.
The symptoms of acidosis can vary depending on the type and severity of the condition. Common symptoms include:
1. Fatigue
2. Weakness
3. Confusion
4. Headaches
5. Nausea and vomiting
6. Abdominal pain
7. Difficulty breathing
8. Rapid heart rate
9. Muscle twitching
If left untreated, acidosis can lead to complications such as:
1. Kidney damage
2. Seizures
3. Coma
4. Heart arrhythmias
5. Respiratory failure
Treatment of acidosis depends on the underlying cause and the severity of the condition. Some common treatments include:
1. Oxygen therapy
2. Medications to help regulate breathing and heart rate
3. Fluid and electrolyte replacement
4. Dietary changes
5. Surgery, in severe cases.
In conclusion, acidosis is a serious medical condition that can have severe consequences if left untreated. It is important to seek medical attention immediately if you suspect that you or someone else may have acidosis. With prompt and appropriate treatment, it is possible to effectively manage the condition and prevent complications.
Example sentence: "The patient was diagnosed with lactic acidosis secondary to uncontrolled diabetes and was admitted to the intensive care unit for proper management."
Some common symptoms of respiratory acidosis include:
* Rapid breathing rate
* Shallow breathing
* Fatigue
* Confusion or disorientation
* Headaches
* Muscle weakness
* Numbness or tingling in the hands and feet
If left untreated, respiratory acidosis can lead to serious complications such as seizures, coma, and even death. Treatment typically involves addressing the underlying cause of the condition, such as surgery for a weakened diaphragm or other breathing muscles, or using mechanical ventilation if necessary.
It is important to seek medical attention if you experience any symptoms of respiratory acidosis, as early diagnosis and treatment can help prevent complications and improve outcomes.
There are several types of RTA, including:
1. Type 1 RTA: This is caused by a defect in the genes that code for the proteins involved in acid secretion in the renal tubules.
2. Type 2 RTA: This is caused by damage to the renal tubules, such as from exposure to certain drugs or toxins.
3. Type 4 RTA: This is caused by a deficiency of the hormone aldosterone, which helps regulate electrolyte levels in the body.
Symptoms of RTA can include:
* Nausea and vomiting
* Abdominal pain
* Fatigue
* Weakness
* Dehydration
* Increased heart rate
* Decreased urine production
RTA can be diagnosed through blood tests that measure the pH levels in the body, as well as tests that assess kidney function and electrolyte levels. Treatment for RTA typically involves correcting any underlying causes, such as stopping certain medications or addressing electrolyte imbalances. In some cases, medications may be prescribed to help regulate acid levels in the body.
Prevention of RTA includes maintaining proper hydration, avoiding exposure to harmful substances, and managing any underlying medical conditions that may increase the risk of developing RTA. Early detection and treatment can help prevent complications and improve outcomes for individuals with RTA.
There are several types of alkalosis, including:
1. Respiratory alkalosis: This type is caused by an excessive breathing of carbon dioxide into the lungs, which increases the bicarbonate levels in the blood.
2. Metabolic alkalosis: This type is caused by a decrease in the production of acid in the body, such as in diabetic ketoacidosis or liver disease.
3. Inherited alkalosis: This type is caused by inherited genetic disorders that affect the regulation of acid-base homeostasis.
4. Drug-induced alkalosis: Certain medications, such as antacids and diuretics, can increase bicarbonate levels in the blood.
5. Post-operative alkalosis: This type can occur after surgery, particularly gastrointestinal surgery, due to the release of bicarbonate from damaged tissues.
The symptoms of alkalosis can vary depending on the severity and duration of the condition. They may include:
* Nausea and vomiting
* Abdominal pain
* Headache
* Fatigue
* Muscle weakness
* Tingling sensations in the extremities
* Confusion and disorientation
If left untreated, alkalosis can lead to more severe complications such as:
* Respiratory acidosis (a decrease in blood pH due to a lack of oxygen)
* Cardiac arrhythmias (irregular heartbeats)
* Seizures
* Coma
Diagnosis of alkalosis is based on a combination of physical examination, medical history, and laboratory tests. Laboratory tests may include:
* Arterial blood gas (ABG) analysis to measure the pH and PCO2 levels in the blood
* Serum electrolyte levels to assess the levels of sodium, potassium, and chloride
* Urine testing to assess the levels of bicarbonate and other electrolytes
Treatment of alkalosis depends on the underlying cause and severity of the condition. General measures may include:
* Correction of any underlying metabolic disorders, such as diabetes or kidney disease
* Discontinuation of medications that may be contributing to the alkalosis
* Fluid and electrolyte replacement to correct dehydration or imbalances
* Oxygen therapy to treat respiratory acidosis
In severe cases, hospitalization may be necessary to monitor and treat the condition. In some cases, medications such as sodium bicarbonate may be prescribed to help restore acid-base balance. Surgery may be required in cases where the alkalosis is caused by a structural problem, such as a hiatal hernia.
Prognosis for alkalosis depends on the underlying cause and severity of the condition. In general, early diagnosis and treatment can improve outcomes. However, untreated severe alkalosis can lead to complications such as seizures, coma, and cardiac arrhythmias.
Prevention of alkalosis involves identifying and treating underlying conditions that may contribute to the development of the condition. This includes managing chronic diseases such as diabetes and kidney disease, and avoiding medications that may cause alkalosis. Additionally, maintaining a balanced diet and staying hydrated can help prevent electrolyte imbalances that can lead to alkalosis.
In conclusion, alkalosis is a condition characterized by an excess of base in the body, which can lead to respiratory and metabolic disturbances. The diagnosis of alkalosis is based on a combination of physical examination, medical history, and laboratory tests. Treatment depends on the underlying cause and severity of the condition, and may include fluid and electrolyte replacement, medication, and addressing any underlying conditions. Early diagnosis and treatment can improve outcomes for patients with alkalosis.
The symptoms of MELAS syndrome can vary in severity and may include:
* Muscle weakness and wasting
* Seizures
* Stroke-like episodes
* Lactic acidosis (a buildup of lactic acid in the blood)
* Encephalopathy (damage to the brain)
* Vision loss
* Hearing loss
* Cognitive impairment
* Behavioral changes
* Autism
The diagnosis of MELAS syndrome is based on a combination of clinical findings, laboratory tests, and genetic analysis. Treatment is focused on managing the symptoms and preventing complications. This may include medications to control seizures, physical therapy to improve muscle strength and function, and dietary changes to manage lactic acidosis.
MELAS syndrome is a rare condition, and there is currently no cure. However, with proper management, individuals with MELAS syndrome can lead relatively normal lives. It is important for individuals with this condition to receive ongoing medical care and monitoring to manage their symptoms and prevent complications.
There are two main types of acid-base imbalances:
1. Respiratory acidosis: This occurs when the body produces too much carbon dioxide, leading to an increase in blood acidity. Causes include chronic obstructive pulmonary disease (COPD), pneumonia, and sleep apnea.
2. Metabolic acidosis: This occurs when the body produces too little base, leading to an increase in blood acidity. Causes include diabetic ketoacidosis, kidney failure, and excessive alcohol consumption.
Symptoms of acid-base imbalance can include:
* Fatigue
* Weakness
* Nausea
* Vomiting
* Headaches
* Confusion
* Coma (in severe cases)
Treatment of acid-base imbalance depends on the underlying cause and may involve corrective measures such as:
* Oxygen therapy
* Medications to restore blood pH balance
* Diuretics to remove excess fluids
* Insulin therapy (for metabolic acidosis)
* Hemodialysis (for severe cases of metabolic acidosis)
It is important for healthcare professionals to monitor and maintain acid-base balance in patients, particularly those with pre-existing medical conditions or those undergoing surgical procedures.
Symptoms of DKA can include:
* High blood sugar levels (usually above 300 mg/dL)
* High levels of ketones in the blood and urine
* Nausea, vomiting, and abdominal pain
* Fatigue, weakness, and confusion
* Headache and dry mouth
* Flu-like symptoms, such as fever, chills, and muscle aches
If left untreated, DKA can lead to serious complications, such as:
* Dehydration and electrolyte imbalances
* Seizures and coma
* Kidney damage and failure
Treatment of DKA typically involves hospitalization and intravenous fluids to correct dehydration and electrolyte imbalances. Insulin therapy is also started to lower blood sugar levels and promote the breakdown of ketones. In severe cases, medications such as sodium bicarbonate may be given to help neutralize the excess ketones in the blood.
Preventing DKA involves proper management of diabetes, including:
* Taking insulin as prescribed and monitoring blood sugar levels regularly
* Maintaining a healthy diet and exercise program
* Monitoring for signs of infection or illness, which can increase the risk of DKA
Early detection and treatment of DKA are critical to preventing serious complications and improving outcomes for people with diabetes.
Hypercapnia is a medical condition where there is an excessive amount of carbon dioxide (CO2) in the bloodstream. This can occur due to various reasons such as:
1. Respiratory failure: When the lungs are unable to remove enough CO2 from the body, leading to an accumulation of CO2 in the bloodstream.
2. Lung disease: Certain lung diseases such as chronic obstructive pulmonary disease (COPD) or pneumonia can cause hypercapnia by reducing the ability of the lungs to exchange gases.
3. Medication use: Certain medications, such as anesthetics and sedatives, can slow down breathing and lead to hypercapnia.
The symptoms of hypercapnia can vary depending on the severity of the condition, but may include:
1. Headaches
2. Dizziness
3. Confusion
4. Shortness of breath
5. Fatigue
6. Sleep disturbances
If left untreated, hypercapnia can lead to more severe complications such as:
1. Respiratory acidosis: When the body produces too much acid, leading to a drop in blood pH.
2. Cardiac arrhythmias: Abnormal heart rhythms can occur due to the increased CO2 levels in the bloodstream.
3. Seizures: In severe cases of hypercapnia, seizures can occur due to the changes in brain chemistry caused by the excessive CO2.
Treatment for hypercapnia typically involves addressing the underlying cause and managing symptoms through respiratory support and other therapies as needed. This may include:
1. Oxygen therapy: Administering oxygen through a mask or nasal tubes to help increase oxygen levels in the bloodstream and reduce CO2 levels.
2. Ventilation assistance: Using a machine to assist with breathing, such as a ventilator, to help remove excess CO2 from the lungs.
3. Carbon dioxide removal: Using a device to remove CO2 from the bloodstream, such as a dialysis machine.
4. Medication management: Adjusting medications that may be contributing to hypercapnia, such as anesthetics or sedatives.
5. Respiratory therapy: Providing breathing exercises and other techniques to help improve lung function and reduce symptoms.
It is important to seek medical attention if you suspect you or someone else may have hypercapnia, as early diagnosis and treatment can help prevent complications and improve outcomes.
Respiratory alkalosis can occur due to various causes such as hypoventilation (breathing too slowly), hypercapnia (excessive carbon dioxide in the blood), bicarbonate therapy, or drinking excessive amounts of antacids. Symptoms may include vomiting, abdominal pain, headache, and muscle weakness.
Treatment typically involves addressing the underlying cause, such as correcting hypoventilation or removing excess carbon dioxide from the bloodstream. In severe cases, medications or mechanical ventilation may be necessary.
The normal range for potassium levels in the blood varies depending on age, gender, and other factors, but generally it is between 3.5 and 5.5 mEq/L (milliequivalents per liter).
Hypokalemia can be caused by a variety of factors such as diarrhea, vomiting, certain medications (diuretics, laxatives), kidney disease or malfunctioning of the parathyroid glands.
Causes of Hyperkalemia:
1. Kidney dysfunction: When the kidneys are not able to excrete excess potassium, it can build up in the bloodstream and lead to hyperkalemia.
2. Medications: Certain drugs, such as ACE inhibitors, potassium-sparing diuretics, and NSAIDs, can increase potassium levels by blocking the excretion of potassium in the urine.
3. Diabetic ketoacidosis: High levels of potassium can occur in people with uncontrolled diabetes who have diabetic ketoacidosis.
4. Acute kidney injury: This condition can cause a rapid increase in potassium levels as the kidneys are unable to remove excess potassium from the blood.
5. Heart disease: Potassium levels can rise in people with heart failure or other cardiac conditions, leading to hyperkalemia.
Symptoms of Hyperkalemia:
1. Muscle weakness and fatigue
2. Abnormal heart rhythms (arrhythmias)
3. Palpitations
4. Constipation
5. Nausea and vomiting
6. Abdominal cramps
7. Fatigue
8. Confusion
9. Headaches
10. Weakness in the legs and feet
Treatment of Hyperkalemia:
The treatment of hyperkalemia depends on the underlying cause and the severity of the condition. Some of the common methods for lowering potassium levels include:
1. Diuretics: These medications help remove excess fluid and electrolytes, including potassium, from the body.
2. Calcium gluconate: This medication can help stabilize cardiac function and reduce the risk of arrhythmias.
3. Insulin and glucose: Giving insulin and glucose to someone with diabetic ketoacidosis can help lower potassium levels by increasing glucose uptake in the cells.
4. Hemodialysis: This is a process that uses a machine to filter waste products, including excess potassium, from the blood.
5. Potassium-binding resins: These medications can bind to potassium ions in the gut and prevent their absorption into the bloodstream.
6. Sodium polystyrene sulfonate (Kayexalate): This medication can help lower potassium levels by binding to excess potassium in the gut and causing it to be eliminated in the stool.
7. Activated charcoal: This medication can help bind to potassium ions in the gut and prevent their absorption into the bloodstream.
In severe cases of hyperkalemia, hospitalization may be necessary to monitor and treat the condition. In some instances, dialysis may be required to remove excess potassium from the blood. It is important to note that the treatment for hyperkalemia should only be done under the guidance of a healthcare professional, as some medications or procedures can worsen the condition if not properly managed.
The symptoms of Fanconi Syndrome can vary in severity and may include:
* Diarrhea
* Dehydration
* Abdominal pain
* Failure to gain weight or grow at the expected rate
* Increased risk of infections
* Poor blood sugar control
* High levels of amino acids in the urine
* Abnormal kidney function
Fanconi Syndrome is usually diagnosed through a combination of clinical evaluation, laboratory tests, and genetic analysis. Treatment for the condition typically involves managing the symptoms and addressing any underlying complications. This may include:
* Nutritional support to ensure adequate intake of essential nutrients
* Hydration to prevent dehydration
* Antibiotics to prevent or treat infections
* Medications to manage diarrhea and abdominal pain
* Monitoring of blood sugar levels
* Kidney function tests to monitor for any kidney damage
There is no cure for Fanconi Syndrome, but with proper management, individuals with the condition can lead relatively normal lives. It is important for individuals with Fanconi Syndrome to receive regular medical care and follow a carefully planned diet to manage their symptoms and prevent complications.
Symptoms of nephrocalcinosis may include nausea, vomiting, abdominal pain, frequent urination, and blood in the urine. Diagnosis is typically made through imaging tests such as X-rays, CT scans, or ultrasound, and blood tests to determine calcium levels and kidney function.
Treatment for nephrocalcinosis depends on the underlying cause of the condition and may include medications to lower calcium levels, dietary changes to reduce calcium intake, and in severe cases, dialysis or kidney transplantation may be necessary. It is important to seek medical attention if symptoms persist or worsen over time, as early detection and treatment can help prevent long-term damage to the kidneys.
Acidosis
Hyperchloremic acidosis
Lactic acidosis
Respiratory acidosis
Metabolic acidosis
Renal tubular acidosis
Congenital lactic acidosis
Normal anion gap acidosis
Proximal renal tubular acidosis
Distal renal tubular acidosis
High anion gap metabolic acidosis
Robert Donald Cohen
Tumor lysis syndrome
Ringer's lactate solution
Wilfrid Payne
Glucocorticoid remediable aldosteronism
Streptococcus bovis
Hyperchloremia
Hyperaldosteronism
Sodium bicarbonate
Exercise intolerance
List of OMIM disorder codes
Adverse effect
Wladimir Wertelecki
Sulfur
Bernhard Naunyn
Cori cycle
Carboxyhemoglobin
Pauline Hald
Ann Stone Minot
Hyperchloremic Acidosis Differential Diagnoses
Acute Lactic Acidosis: Overview, Treatment Overview, Prehospital Care
Acidosis: MedlinePlus Medical Encyclopedia
Zonisamide : metabolic acidosis
Sodium Bicarbonate in Severe Metabolic Acidosis
Lactic Acidosis Traced to Thiamine Deficiency Related to
Nationwide Shortage of Multivitamins for Total Parenteral
Nutrition ...
acidosis | Taber's Medical Dictionary
HIE Multimedia - Metabolic acidosis
WHO EMRO | Case reports: Unusual association between renal tubular acidosis and Chilaiditi syndrome: a case report | Volume 12,...
Acidosis while Dieting
MeSH | Acidosis (D000138)
acidosis | ward round stuff
Metabolic Acidosis | Nursing Tutorials
respiratory acidosis
Respiratory Acidosis Vs Alkalosis | DiabetesTalk.Net
Lactic Acidosis Causes & Treatment - Free eBook
Sub acute ruminal acidosis Archives - Dairy Global
Lactic Acidosis Treatment You Should Try | Healthcare-Online
Details for:
Metabolic acidosis.
› WHO HQ Library catalog
Metformin-associated lactic acidosis in patients with renal insufficiency
Bicarbonate Therapy for Critically Ill Patients with Metabolic Acidosis: A Systematic Review. | Cureus;11(3): e4297, 2019 Mar...
Functional photoacoustic microscopy for high-resolution and noninvasive in vivo imaging | Nature Biotechnology
MITOCHONDRIAL MYOPATHY, ENCEPHALOPATHY, LACTIC ACIDOSIS, AND STROKE-LIKE EPISODES; MELAS | MENDELIAN.CO
Impaired consciousness, hypokalaemia and renal tubular acidosis in sustained Nurofen Plus abuse. | MediFind
Common Diseases in India - Prevention and Cure of Common Diseases in children and adults.
Acid-Base Balance: How Does It Affect Your Health?
Renal histopathology of stone-forming patients with distal renal tubular acidosis<...
INTERNAL MEDICINE | MindMeister Mind Map
A Quick Reference on Hyperchloremic Metabolic Acidosis. | Carlson College of Veterinary Medicine | Oregon State University
1355. Four causes of lactic acidosis // Two types of RTA // Physiologic responses to acidemia - emupdates
Lactic38
- Lactic acidosis (LA), identified by an accumulation of plasma lactate concentration, is one type of anion gap metabolic acidosis and may manifest from numerous conditions. (medscape.com)
- [ 2 , 4 , 5 ] Clinical context and severity govern the effect of lactic acidosis, with mortality increasing by a factor of about three when the condition is associated with sepsis or low-flow states. (medscape.com)
- Lactic acidosis remains the most common cause of metabolic acidosis in hospitalized patients. (medscape.com)
- Lactic acidosis is characterized by an excess of serum lactate when lactate production is augmented, lactate utilization and clearance are decreased, or both. (medscape.com)
- Treatment with buffering agents for acute lactic acidosis remains controversial. (medscape.com)
- Dialysis may also be useful when severe lactic acidosis exists in the setting of renal failure or congestive heart failure, as well as with severe metformin intoxication. (medscape.com)
- Several studies related to metformin-related lactic acidosis and acute kidney failure found significantly reduced morbidity and mortality related to continuous renal replacement therapy (CRRT) or hemodialysis. (medscape.com)
- Lactic acidosis is a buildup of lactic acid . (medlineplus.gov)
- Many causes of metabolic acidosis can be prevented, including diabetic ketoacidosis and some causes of lactic acidosis. (medlineplus.gov)
- This report describes three patients receiving TPN who had thiamine deficiency-related lactic acidosis in 1997 and presents recommendations for alternatives to parenteral MVI during the shortage. (cdc.gov)
- Lactic acidosis of unknown etiology was diagnosed, and broad-spectrum antimicrobials were initiated after appropriate cultures were obtained. (cdc.gov)
- In general, when blood pH is less than 7.35 and lactate is greater than 5 to 6 mmol/L (5 to 6 mEq/L), lactic acidosis is present. (tabers.com)
- STEP 2: MECHANISM of Chronic Disease = there is one single most common mechanism of chronic disease and it is called Lactic Acidosis. (thenutritionalhealingcenter.com)
- It's all about feeding, strengthening and supporting your organs to reverse engineer your lactic acidosis and stop it from killing your cells and flip over to the most important fuel, ketones. (thenutritionalhealingcenter.com)
- Click below to download your Free eBook on lactic acidosis causes and treatment. (thenutritionalhealingcenter.com)
- Lactic acidosis is a medical condition caused mainly due to the excess lactic acid in your blood. (healthcare-online.org)
- It is important to identify the exact cause to find the right treatment for lactic acidosis. (healthcare-online.org)
- Keep reading to discover more about some of the most common causes of lactic acidosis and some possible lactic acidosis treatment options. (healthcare-online.org)
- What Is Lactic Acidosis? (healthcare-online.org)
- In order to find the most appropriate treatment for lactic acidosis, you need to understand exactly what it is and what causes it in the first place. (healthcare-online.org)
- 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)
- The acid keeps building in your body and leads to lactic acidosis. (healthcare-online.org)
- 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)
- You need to inform your healthcare provider of your symptoms so they could select the best treatment of lactic acidosis. (healthcare-online.org)
- In case of severe lactic acidosis, it is important to take the patient to the hospital without wasting any time. (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 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)
- 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)
- Go see your doctor if you notice any symptoms related to lactic acidosis. (healthcare-online.org)
- What lactic acidosis treatment is right for you usually depends on your lactate value. (healthcare-online.org)
- They will, however, stop your HIV drugs when the value goes beyond 5mmol/dL - this is only when you also have specific symptoms of lactic acidosis. (healthcare-online.org)
- If you're taking HIV drugs, you should never stop using them without informing your doctor because HIV drug plays a big role in lactic acidosis. (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)
- 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)
- MELAS (Mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke) syndrome is a rare progressive multisystemic disorder characterized by encephalomyopathy, lactic acidosis, and stroke-like episodes. (mendelian.co)
- Melas Is also known as mitochondrial encephalomyopathy, lactic acidosis and stroke-like episodes, melas syndrome, mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes. (mendelian.co)
- Juvenile myopathy, encephalopathy, lactic acidosis AND stroke. (mendelian.co)
Distal renal tubular5
- The genetic and clinical spectrum of a large cohort of patients with distal renal tubular acidosis. (medscape.com)
- Distal renal tubular acidosis. (medscape.com)
- Prevalence of distal renal tubular acidosis in patients with calcium phosphate stones. (medscape.com)
- Kidney disease (uremia, distal renal tubular acidosis or proximal renal tubular acidosis ). (medlineplus.gov)
- To define the renal tissue changes in stone-forming patients with distal renal tubular acidosis (dRTA), we performed intra-operative papillary and cortical biopsies in five patients. (johnshopkins.edu)
Hypokalaemia and metabolic acidosis2
- His past history was significant for severe duodenitis, chronic diarrhoea, hypokalaemia and metabolic acidosis. (who.int)
- Ibuprofen-induced renal tubular acidosis is a rare but important diagnosis which should be considered in patients presenting with hypokalaemia and metabolic acidosis. (medifind.com)
Carbon dioxide acidosis1
- Other names for respiratory acidosis are hypercapnic acidosis and carbon dioxide acidosis. (medlineplus.gov)
Cause metabolic acidosis1
- Seek medical help if you have symptoms of any disease that can cause metabolic acidosis. (adam.com)
Hyperchloremic metabolic acidosis3
- A Quick Reference on Hyperchloremic Metabolic Acidosis. (oregonstate.edu)
- Metabolic acidosis is divided into hyperchloremic metabolic acidosis and high anion gap acidosis based on the changes in the anion gap. (oregonstate.edu)
- Hyperchloremic metabolic acidosis is the result of chloride retention, excessive loss of sodium relative to chloride, or excessive gain of chloride relative to sodium. (oregonstate.edu)
Loss of bicarbonate1
- An actual or relative increase in the acidity of blood due to an accumulation of acids (as in diabetic acidosis or renal disease) or an excessive loss of bicarbonate (as in renal disease). (tabers.com)
Clinical3
- Clinical features, genetic background, and outcome in infants with urinary tract infection and type IV renal tubular acidosis. (medscape.com)
- Respiratory acidosis is a serious clinical complication that can be potentially fatal. (iloveindia.com)
- Clinical signs are related to the underlying disease that accompanies the metabolic acidosis. (oregonstate.edu)
Etiology1
- The underlying etiology of metabolic acidosis is classically categorized into those causes that result in an elevated anion gap (AG) (see the Anion Gap calculator) and those that do not. (medscape.com)
Acute5
- Kraut JA, Kurtz I. Treatment of acute non-anion gap metabolic acidosis. (medscape.com)
- Toyonaga Y, Kikura M. Hyperchloremic acidosis is associated with acute kidney injury after abdominal surgery. (medscape.com)
- In the acute state, respiratory compensation of acidosis occurs by hyperventilation resulting in a relative reduction in the partial pressure of carbon dioxide (PaCO 2 ). (medscape.com)
- The current literature suggests limited benefit from bicarbonate therapy for patients with severe metabolic acidosis ( pH bicarbonate bicarbonate therapy does yield improvement in survival for patients with accompanying acute kidney injury . (bvsalud.org)
- Primary Sjögren syndrome-associated acute interstitial nephritis and type 3 renal tubular acidosis in a patient with thin basement membrane nephropathy: A case report. (medifind.com)
Diabetic1
- Diabetic acidosis (also called diabetic ketoacidosis and DKA) develops when substances called ketone bodies (which are acidic) build up during uncontrolled diabetes . (medlineplus.gov)
Symptoms5
- Metabolic acidosis symptoms depend on the underlying disease or condition. (medlineplus.gov)
- All the types of acidosis will cause symptoms that require treatment by your provider. (medlineplus.gov)
- Most symptoms are caused by the underlying disease or condition that is causing the metabolic acidosis. (adam.com)
- Acidosis has several symptoms, including headache and confusion, and the individual can become lethargic and easily fatigued. (diabetestalk.net)
- If your metabolic acidosis is mild, you may not have any symptoms. (webmd.com)
Alkalosis5
- Effects of Respiratory Acidosis and Alkalosis on the Distribution of Cyanide into the Rat Brain, Toxicological Sciences, Volume 61, Issue 2, 1 June 2001, Pages 273282, The aim of this study was to determine whether respiratory acidosis favors the cerebral distribution of cyanide, and conversely, if respiratory alkalosis limits its distribution. (diabetestalk.net)
- Home / ABA Keyword Categories / A / ABG: Respiratory acidosis/metabolic alkalosis ABG: Respiratory acidosis/metabolic alkalosis A combined respiratory acidosis / metabolic alkalosis will result in elevated PaCO2 and serum bicarbonate. (diabetestalk.net)
- Which process is the primary disorder (e.g. primary respiratory acidosis with metabolic compensation versus primary metabolic alkalosis with respiratory compensation) is dependent on the pH in an acidotic patient, the acidosis is primary (and the alkalosis is compensatory) and vice versa. (diabetestalk.net)
- Both acidosis and alkalosis can be caused by either metabolic or respiratory disorders. (diabetestalk.net)
- Acidosis and alkalosis aren't diseases, but they provide health care professionals with a clue that you may have a serious health problem. (webmd.com)
Encephalopathy1
- Threshold of metabolic acidosis associated with neonatal encephalopathy in the term newborn. (bvsalud.org)
Nonanion1
- Nonanion gap metabolic acidoses occur in diarrhea, renal tubular acidosis, and multiple myeloma. (tabers.com)
Autoimmune diseases1
- The causes of renal tubular acidosis include hereditary disorders, autoimmune diseases and certain drugs such as amphotericin B, lithium and analgesics. (who.int)
Dehydration1
- Fetal death may occur due to fetal hypoxia and acidosis resulting from excessive maternal dehydration. (cdc.gov)
Excessive1
- The diagnosis of renal tubular acidosis had been considered and subsequent disclosure of excessive chronic ingestion of ibuprofen suggested this to be the underlying cause. (medifind.com)
Occurs3
- Acidosis occurs when acid builds up or when bicarbonate (a base) is lost. (medlineplus.gov)
- Compensated acidosis occurs when the body returns the acid-base balance to near normal in cases of acidosis, but bicarbonate and carbon dioxide levels remain abnormal. (medlineplus.gov)
- Acidosis occurs when blood pH decreases . (diepta.de)
Abnormal1
- Metabolic acidosis is usually categorized by the presence or absence of an abnormal anion gap. (tabers.com)
Acidotic1
- If you have an anion gap, then youve automatically got a little bit of an acidosis on top of the compensation (because the compensation should be a NON-gap acidotic process. (diabetestalk.net)
Diagnosis1
- The presence of metabolic acidosis with anion and osmolal gaps is an important clue to the diagnosis (Friedman et al. (cdc.gov)
Kidneys1
- Normally, people with healthy kidneys and lungs do not have serious acidosis. (medlineplus.gov)
Dialysis1
- Metabolic acidosis due to prolonged hemodialysis in which the pH of the dialysis bath has been inadvertently reduced by the action of contaminating bacteria. (tabers.com)
Acids2
- Acidosis arises from an increased production of acids, a loss of alkali, or a decreased renal excretion of acids. (medscape.com)
- and acidoses that result from the consumption of excess acids e.g., salicylates, methanol, or ethanol. (tabers.com)
Bicarbonate Therapy3
- Bicarbonate Therapy for Critically Ill Patients with Metabolic Acidosis: A Systematic Review. (bvsalud.org)
- In this systematic review , we discuss the concept and some specific aspects of bicarbonate therapy for critically ill patients with metabolic acidosis (i.e., patients with blood pH (bvsalud.org)
- We conducted a systematic literature review of three online databases ( PubMed , Google Scholar, and Cochrane) in November 2018 to validate usage of bicarbonate therapy for critically ill patients with metabolic acidosis . (bvsalud.org)
Patient's1
- This case report describes a 33-year-old woman diagnosed with ibuprofen-induced renal tubular acidosis treated with correction of the patient's electrolyte and acid-base disturbance. (medifind.com)
Sodium2
- Hyperchloremic acidosis is caused by the loss of too much sodium bicarbonate from the body, which can happen with severe diarrhea. (medlineplus.gov)
- These images are a random sampling from a Bing search on the term "Sodium Bicarbonate in Severe Metabolic Acidosis. (fpnotebook.com)
Patients1
- An anion gap metabolic acidosis in patients with malabsorption, e.g., secondary to short gut syndrome or jejunoileal bypass. (tabers.com)
Mild1
- In some situations, metabolic acidosis can be a mild, ongoing (chronic) condition. (adam.com)
Disorder1
- X-rays of his chest showed fluid in the lungs (pulmonary edema), and bloodwork revealed an acid-base disorder (respiratory and metabolic acidosis). (cdc.gov)
Complication1
- To our knowledge, the development of Chilaiditi syndrome as a complication of severe hypokalaemia from renal tubular acidosis has not been reported in the English language literature. (who.int)
Treatment2
- Treatment is aimed at the health problem causing the acidosis. (adam.com)
- Treatment of hyperchloremic acidosis is based on addressing the underlying disease process. (oregonstate.edu)
Type3
- This type of acidosis is usually caused when the body is unable to remove enough carbon dioxide through breathing. (medlineplus.gov)
- Complications depend on the specific type of acidosis. (medlineplus.gov)
- In this case, the cause of ileus was severe hypokalaemia resulting from type-1 renal tubular acidosis. (who.int)
Acid-base1
- Metabolic acidosis is mainly caused by an imbalance of the body's acid-base balance. (diepta.de)
Recipients1
- Kaneko S, Usui J, Takahashi K, Oda T, Yamagata K. Increased intrarenal post-glomerular blood flow is a key condition for the development of calcineurin inhibitor-induced renal tubular acidosis in kidney transplant recipients. (medscape.com)
