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Metabolic acidosis is a serious electrolyte disorder characterized by an imbalance in the body's acid-base balance.Metabolic acidosis has three main root causes: increased acid production, loss of bicarbonate, and a reduced ability of the kidneys to excrete excess acids. [5]
In general, the cause of a hyperchloremic metabolic acidosis is a loss of base, either a gastrointestinal loss or a renal loss [citation needed]. Gastrointestinal loss of bicarbonate (HCO − 3) [citation needed] Severe diarrhea (vomiting will tend to cause hypochloraemic alkalosis) Pancreatic fistula with loss of bicarbonate rich pancreatic fluid
Hyperparathyroidism – can cause hyperchloremia and increase renal bicarbonate loss, which may result in a normal anion gap metabolic acidosis. Patients with hyperparathyroidism may have a lower than normal pH, slightly decreased PaCO2 due to respiratory compensation, a decreased bicarbonate level, and a normal anion gap.
High anion gap metabolic acidosis is a form of metabolic acidosis characterized by a high anion gap (a medical value based on the concentrations of ions in a patient's serum). Metabolic acidosis occurs when the body produces too much acid , or when the kidneys are not removing enough acid from the body.
Metabolic acidosis is compensated for in the lungs, as increased exhalation of carbon dioxide promptly shifts the buffering equation to reduce metabolic acid. This is a result of stimulation to chemoreceptors , which increases alveolar ventilation , leading to respiratory compensation, otherwise known as Kussmaul breathing (a specific type of ...
Hypoaldosteronism causes low sodium (hyponatremia), high potassium (hyperkalemia), and metabolic acidosis, a condition in which the body produces excess acid.These conditions are responsible for the symptoms of hypoaldosteronism, which include muscle weakness, nausea, palpitations, irregular heartbeat, and abnormal blood pressure.
Methylmalonic acidemia has an autosomal recessive pattern of inheritance.. Methylmalonic acidemias have an autosomal recessive inheritance pattern, which means the defective gene is located on an autosome, and two copies of the gene—one from each parent—must be inherited to be affected by the disorder.
Renal tubular acidosis (RTA) is a medical condition that involves an accumulation of acid in the body due to a failure of the kidneys to appropriately acidify the urine. [1] In renal physiology, when blood is filtered by the kidney, the filtrate passes through the tubules of the nephron, allowing for exchange of salts, acid equivalents, and other solutes before it drains into the bladder as urine.