The term metabolic acidosis refers to all other types of acidosis besides those caused by excess CO2 in the body fluids. Metabolic acidosis can result from several general causes: (1) failure of the kidneys to excrete metabolic acids normally formed in the body, (2) formation of excess quantities of metabolic acids in the body, (3) addition of metabolic acids to the body by ingestion or infusion of acids, and (4) loss of base from the body fluids, which has the same effect as adding an acid to the body fluids. Some specific conditions that cause metabolic acidosis are the following.
Renal Tubular Acidosis. This type of acidosis results from a defect in renal secretion of H+ or in reabsorption of HCO3-, or both. These disorders are generally of two types: (1) impairment of renal tubular HCO3- reabsorption, causing loss of HCO3- in the urine, or (2) inability of the renal tubular H+ secretory mechanism to establish a normal acidic urine, causing the excretion of an alkaline urine. In these cases, inadequate amounts of titratable acid and NH4+ are excreted, so that there is net accumulation of acid in the body fluids. Some causes of renal tubular acidosis include chronic renal failure, insufficient aldosterone secretion (Addison's disease), and several hereditary and acquired disorders that impair tubular function, such as Fanconi's syndrome.
Diarrhea. Severe diarrhea is probably the most frequent cause of metabolic acidosis. The cause of this acidosis is the loss of large amounts of sodium bicarbonate into the feces. The gastrointestinal secretions normally contain large amounts of bicarbonate, and diarrhea results in the loss of HCO3- from the body, which has the same effect as losing large amounts of bicarbonate in the urine. This form of metabolic acidosis is particularly serious and can cause death, especially in young children.
Vomiting of Intestinal Contents. Vomiting of gastric contents alone would cause loss of acid and a tendency toward alkalosis because the stomach secretions are highly acidic. However, vomiting large amounts from deeper in the gastrointestinal tract, which sometimes occurs, causes loss of bicarbonate and results in metabolic acidosis in the same way that diarrhea causes acidosis.
Diabetes Mellitus. Diabetes mellitus is caused by lack of insulin secretion by the pancreas (type I diabetes) or by insufficient insulin secretion to compensate for decreased sensitivity to the effects of insulin (type II diabetes). In the absence of sufficient insulin, the normal use of glucose for metabolism is prevented. Instead, some of the fats are split into acetoacetic acid, and this is metabolized by the tissues for energy in place of glucose.With severe diabetes mellitus, blood acetoacetic acid levels can rise very high, causing severe metabolic acidosis. In an attempt to compensate for this acidosis, large amounts of acid are excreted in the urine, sometimes as much as 500 mmol/day.
Ingestion of Acids. Rarely are large amounts of acids ingested in normal foods. However, severe metabolic acidosis occasionally results from the ingestion of certain acidic poisons. Some of these include acetylsali-cylics (aspirin) and methyl alcohol (which forms formic acid when it is metabolized).
Chronic Renal Failure. When kidney function declines markedly, there is a buildup of the anions of weak acids in the body fluids that are not being excreted by the kidneys. In addition, the decreased glomerular filtration rate reduces the excretion of phosphates and NH4+, which reduces the amount of bicarbonate added back to the body fluids. Thus, chronic renal failure can be associated with severe metabolic acidosis.
Metabolic Alkalosis Is Caused by Increased Extracellular Fluid Bicarbonate Concentration
When there is excess retention of HCO3- or loss of H+ from the body, this results in metabolic alkalosis. Metabolic alkalosis is not nearly as common as metabolic aci-dosis, but some of the causes of metabolic alkalosis are as follows.
Administration of Diuretics (Except the Carbonic Anhydrase Inhibitors). All diuretics cause increased flow of fluid along the tubules, usually causing increased flow in the distal and collecting tubules. This leads to increased reabsorption of Na+ from these parts of the nephrons. Because the sodium reabsorption here is coupled with H+ secretion, the enhanced sodium reabsorption also leads to an increase in H+ secretion and an increase in bicarbonate reabsorption. These changes lead to the development of alkalosis, characterized by increased extracellular fluid bicarbonate concentration.
Excess Aldosterone. When large amounts of aldosterone are secreted by the adrenal glands, a mild metabolic alkalosis develops. As discussed previously, aldosterone promotes extensive reabsorption of Na+ from the distal and collecting tubules and at the same time stimulates the secretion of H+ by the intercalated cells of the collecting tubules. This increased secretion of H+ leads to its increased excretion by the kidneys and, therefore, metabolic alkalosis.
Vomiting of Gastric Contents. Vomiting of the gastric contents alone, without vomiting of the lower gastrointestinal contents, causes loss of the HCl secreted by the stomach mucosa. The net result is a loss of acid from the extracellular fluid and development of metabolic alka-losis. This type of alkalosis occurs especially in neonates who have pyloric obstruction caused by hypertrophied pyloric sphincter muscles.
Ingestion of Alkaline Drugs. A common cause of metabolic alkalosis is ingestion of alkaline drugs, such as sodium bicarbonate, for the treatment of gastritis or peptic ulcer.
The best treatment for acidosis or alkalosis is to correct the condition that caused the abnormality. This is often difficult, especially in chronic diseases that cause impaired lung function or kidney failure. In these circumstances, various agents can be used to neutralize the excess acid or base in the extracellular fluid.
To neutralize excess acid, large amounts of sodium bicarbonate can be ingested by mouth. The sodium bicarbonate is absorbed from the gastrointestinal tract into the blood and increases the bicarbonate portion of the bicarbonate buffer system, thereby increasing pH toward normal. Sodium bicarbonate can also be infused intravenously, but because of the potentially dangerous physiologic effects of such treatment, other substances are often used instead, such as sodium lactate and sodium gluconate. The lactate and gluconate portions of the molecules are metabolized in the body, leaving the sodium in the extracellular fluid in the form of sodium bicarbonate and thereby increasing the pH of the fluid toward normal.
For the treatment of alkalosis, ammonium chloride can be administered by mouth. When the ammonium chloride is absorbed into the blood, the ammonia portion is converted by the liver into urea. This reaction liberates HCl, which immediately reacts with the buffers of the body fluids to shift the H+ concentration in the acidic direction. Ammonium chloride occasionally is infused intravenously, but NH4+ is highly toxic, and this procedure can be dangerous. Another substance used occasionally is lysine monohydrochloride.
Clinical Measurements and Analysis of Acid-Base Disorders
Appropriate therapy of acid-base disorders requires proper diagnosis. The simple acid-base disorders described previously can be diagnosed by analyzing three measurements from an arterial blood sample: pH, plasma bicarbonate concentration, and Pco2.
The diagnosis of simple acid-base disorders involves several steps, as shown in Figure 30-10. By examining the pH, one can determine whether the disorder is acidosis or alkalosis. A pH less than 7.4 indicates acidosis, whereas a pH greater than 7.4 indicates alkalosis.
Arterial blood sample
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Diabetes is a disease that affects the way your body uses food. Normally, your body converts sugars, starches and other foods into a form of sugar called glucose. Your body uses glucose for fuel. The cells receive the glucose through the bloodstream. They then use insulin a hormone made by the pancreas to absorb the glucose, convert it into energy, and either use it or store it for later use. Learn more...